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Anti-inflammatory Effects of Omega 3 and Omega 6 Polyunsaturated Fatty Acids in Cardiovascular Disease and Metabolic Syndrome
Abstract
A lipid excess produces a systemic inflammation process due to tumor necrosis factor-α, interleukin-6 and C-reactive protein synthesis. Simultaneously, this fat excess promotes the appearance of insulin resistance. All this contributes to the development of atherosclerosis and increases the risk of cardiovascular diseases. On the other hand, polyunsaturated fatty acids (PUFAs), especially eicosapentaenoic acid and docosahexaenoic acid (omega 3), and arachidonic acid (omega 6) have shown anti-inflammatory properties. Lately, an inverse relationship between omega-3 fatty acids, inflammation, obesity and cardiovascular diseases has been demonstrated. To check fatty acids effect, the levels of some inflammation biomarkers have been analyzed. Leptin, adiponectin and resistin represent a group of hormones associated with the development of cardiovascular diseases, obesity, type 2 diabetes mellitus and insulin resistance and are modified in obese-overweight people comparing to normal weight people. Omega-3 PUFAs have been shown to decrease the production of inflammatory mediators, having a positive effect in obesity and diabetes mellitus type-2. Moreover, they significantly decrease the appearance of cardiovascular disease risk factors. Regarding omega-6 PUFA, there is controversy whether their effects are pro- or anti-inflammatory. The aim of this manuscript is to provide a comprehensive overview about the role of omega-3 and omega-6 PUFAs in cardiovascular diseases and metabolic syndrome.
... Рис. 5. Мікропрепарати тканини печінки сирійських хом'яків з експериментальним метаболічним синдромом і внутрішньошлунковим введенням комплексної фармацевтичної композиції (28,5 селеном. Так, зокрема встановлена здатність етилових ефірів омега3 кислот включатися в модуляцію ліпідного обміну, регуляцію адипо кінів (адипонектину та лептину), полегшувати перебіг запалення жирової тканини та сприяти адипо генезу зі змінами епігенетичних механізмів [26][27][28]. ...
... Рис. 5. Мікропрепарати тканини печінки сирійських хом'яків з експериментальним метаболічним синдромом і внутрішньошлунковим введенням комплексної фармацевтичної композиції (28,5 селеном. Так, зокрема встановлена здатність етилових ефірів омега3 кислот включатися в модуляцію ліпідного обміну, регуляцію адипо кінів (адипонектину та лептину), полегшувати перебіг запалення жирової тканини та сприяти адипо генезу зі змінами епігенетичних механізмів [26][27][28]. Вітамін Е при гнічує активність ферменту, який бере участь у синтезі холестерину [16]. Коензим Q10, цинк, вітамін А, біотин і селен здатні впливати на регуляцію ліпідного обміну за раху нок реалізації прямої та непрямої антиоксидантної дії, здатності при гнічувати субхронічний запальний процес в організмі [29][30][31][32][33]. ...
Питання застосування вітамінів, вітаміноподібних речовин і мікроелементів хворими з неалкогольною жировою хворобою печінки (НАЖХП) та іншими неінфекційними захворюваннями печінки є дискутабельним.Мета дослідження – встановити вплив комплексної фармацевтичної композиції (Aevit premium) на структуру тканини печінки за умов експериментального метаболічного синдрому (ЕМС) в сирій- ських золотавих хом’яків.Метаболічний синдром у сирійських золотавих хом’яків спричиняли кафе-дієтою, складовими якої були суміш з промислово-оброблених харчових продуктів з вмістом жирів не менше 40 %. Приготовлену суміш давали тваринам з надлишком упродовж 7 тижнів (49 днів). Питну воду було замінено на 10 % розчин фруктози. Досліджувану комплексну фармацевтичну композицію (КФК) Aevit premium (25,8 мг/кг) та препарати порівняння метформін (60,0 мг/кг) і вітамін Е (100 мг/кг) застосовували, починаючи з 5 тижня ЕМС упродовж 3 тижнів (21 день), тобто у лікувальному режимі.Тривале перебування сирійських хом’яків на дієті викликало в тканині печінки ознаки стеатогепатиту: дифузну вакуольну (переважно гідропічну та жирову) дистрофію, запальну круглоклітинну інфільтрацію, накопичення дрібних крапель жиру та значне зменшення насиченості гепатоцитів глікогеном. Під дією КФК спостерігалося зменшення проявів стеатогепатиту в хом’яків з ЕМС. Встановлений позитивний вплив КФК на структуру тканини печінки хом’яків за умов ЕМС ймовірно зумовлений фармакологічними властивостями складових КФК: етиловими ефірами Омега-3 кислот, вітаміном Е, коензимом Q10, цинком, вітаміном А, біотином, селеном. За виразністю коригуючого впливу на стан печінки хом’яків в умовах ЕМС КФК не поступається препаратам порівняння вітаміну Е та метформіну.Отримані результати свідчать про гепатопротекторні властивості КФК за ЕМС.
... Recently, the increasing consumer demands for good food quality, driven by improved living standards, have led to the rising popularity of functional foods, such as those abundant in n-3 PUFAs. Studies have demonstrated that n-3 PUFAs can prevent cardiovascular diseases, such as hypertension and hyperlipidemia [7], promote nervous system development [8], and improve anti-inflammatory and antioxidant responses [9,10]. DHA, especially, plays a vital role in maintaining normal brain development and function [11]. ...
... High triglyceride and high cholesterol contents in plasma are potentially dangerous to human health and are major risk factors for cardiovascular disease [9,20]. The effect of n-3 PUFA on blood lipid levels has been extensively studied in human clinical practice [20], and the hypolipidemic effect of n-3 PUFA has also been observed in broilers [14,19] and ducks [21,22]. ...
The objective of this study is to determine the effects of the dietary replacement of soybean oil (SO) with rubber seed oil (RSO) on the growth performance, carcass trait, and lipid metabolism in Pekin ducks. A total of 160 1-day-old Pekin ducks were randomly allocated to four experimental treatments and fed diets with different ratios of SO to RSO as follows: 3:0 (control), 2:1, 1:2, and 0:3. Dietary RSO supplementation had no effect on their growth performance; however, it significantly decreased the yield of abdominal fat (p < 0.05). As the dietary RSO increased, the plasma TG, CHO, LDL-C, and HDL-C contents of ducks decreased (p < 0.05). Additionally, the contents of total fat, triglycerides, and cholesterol in the liver and breast reduced in the ducks fed RSO diets (p < 0.05). Liver n-3 PUFA levels linearly increased (p < 0.05), while the n-6/n-3 PUFA ratios reduced with increasing RSO levels (p < 0.05). Moreover, dietary RSO supplementation resulted in decreased gene expressions of FABP1, ME1, SREBP1c, FASN, DGAT2, and HMGCR (p < 0.05), while there was an increased expression of the ABCA1 gene (p < 0.05) in the liver of the ducks. In conclusion, dietary RSO supplementation reduced fat deposition and enhanced n-3 PUFA levels without affecting the growth performance of Pekin ducks.
... N-3 fatty acids have been shown to reduce inflammation, prevent cardiovascular disease, support brain function, maintain healthy cholesterol profiles, support the immune system, and reduce obesity [113,115,116]. Insufficient levels of essential fatty acids and an imbalance of the n-3/n-6 fatty acid ratio are associated with dyslipidemia, high blood pressure, heart disease, and an increased risk for premature death in the population without SCI [117]. ...
... N -6 fatty acids are involved in the regulation of energy production as part of metabolism, as well as the maintenance of skin, bone, and hair health [125]. Although n-6 fatty acids are vital for several physiological functions, their effect on cardiovascular health remains unclear [116,125]. Some evidence indicates that an increased intake of n-6 fatty acids can lower cardiovascular disease risk by reducing total serum cholesterol, lowering blood pressure, improving insulin resistance, and reducing incidence of diabetes mellitus [125][126][127]. ...
Spinal cord injury (SCI) results in a high prevalence of neurogenic obesity and metabolic dysfunction. The increased risk for neurogenic obesity and metabolic dysfunction is mainly due to the loss of energy balance because of significantly reduced energy expenditure following SCI. Consequently, excessive energy intake (positive energy balance) leads to adipose tissue accumulation at a rapid rate, resulting in neurogenic obesity, systemic inflammation, and metabolic dysfunction. The purpose of this article is to review the existing literature on nutrition, dietary intake, and nutrition education in persons with SCI as it relates to metabolic dysfunction. The review will highlight the poor dietary intakes of persons with SCI according to authoritative guidelines and the need for nutrition education for health care professionals and consumers. Nutrition education topics are presented in a module-based format with supporting literature. The authors emphasize the role of a diet consisting of low-energy, nutrient-dense, anti-inflammatory foods consistent with the Dietary Guidelines for Americans’ MyPlate to effectively achieve energy balance and reduce the risk for neurogenic obesity and metabolic dysfunction in individuals with SCI.
... Furthermore, the content and composition of fatty acids in muscle play a key role in meat quality, which determines the nutritional value and flavor of the meat. Previous studies have demonstrated that polyunsaturated fatty acids (PUFA) are tied to anti-obesity and anti-inflammatory properties, particularly n-3 PUFA (Buckley and Howe, 2009;Tortosa-Caparr os et al., 2017). Nutritional regulation is an effective means to improve pork quality. ...
... The fatty acid profiles in the IMF determine the nutritional value and oxidative stability of muscle and are particularly important for meat quality and meat product acceptability (Duan et al., 2016). A high intake of SFAs has been reported to increase the risk of type-2 diabetes (T2D) and heart disease (Lenighan et al., 2019), while PUFA, in particular EPA and DHA, have been found to possess numerous benefits, such as anti-inflammatory, glycolipid metabolism regulation and muscle development properties (Tachtsis et al., 2018;Tortosa-Caparr os et al., 2017;Vaidya and Cheema, 2014;Vissers et al., 2019). In the current study, only 10% FMF supplementation increased the content of PUFA and the PUFA:SFA ratio. ...
This study was conducted to investigate the effects of fermented mixed feed (FMF) on growth performance, carcass traits, meat quality, muscle amino acid and fatty acid composition and mRNA expression levels of genes related to lipid metabolism in finishing pigs. In the present study, 144 finishing pigs (Duroc × Berkshire × Jiaxing Black) were randomly allocated to 3 dietary treatments with 4 replicate pens per group and 12 pigs per pen. The dietary treatments included a basal diet (CON), a basal diet + 5% FMF and a basal diet + 10% FMF. The experiment lasted 38 d after 4 d of acclimation. The results showed that 5% and 10% FMF significantly increased the average daily gain (ADG) of the females but not the males (P < 0.05), but FMF supplementation showed no impact on carcass traits. Moreover, 10% FMF supplementation increased the meat color45 min and meat color24 h values, while it decreased the shear force relative to CON (P < 0.05). In addition, 10% FMF significantly increased the contents of flavor amino acids (FAA), total essential AA (EAA), total non-EAA (NEAA) and total AA relative to CON (P < 0.05). Furthermore, the diet supplemented with 10% FMF significantly increased the concentration of n-3 polyunsaturated fatty acids (PUFA), n-6 PUFA and total PUFA, and the PUFA:SFA ratio (P < 0.05), suggesting that FMF supplementation increased meat quality. Moreover, compared with the CON, 10% FMF supplementation increased the mRNA expression of lipogenic genes, including CEBPα, PPARγ, SREBP1 and FABP4, and upregulated the expression of unsaturated fatty acid synthesis (ACAA1 and FADS2). Together, our results suggest that 10% FMF dietary supplementation improved the female pigs’ growth performance, improved the meat quality and altered the profiles of muscle fatty acids and amino acids in finishing pigs. This study provides a reference for the production of high-quality pork.
... Basically, the daily energy supply of the patients should be through protein, fat, and carbohydrates. To measure individual calorie requirements, indirect calorimetry has developed into the gold standard [38]. In practice, the rule of thumb of 25-30 kcal/kg body weight has proven itself [4], but there are also differences here with regard to the determined and the recommended energy requirement [37]. ...
... As is well known, the use of high-quality vegetable oils can have a positive effect on inflammation. Consequently, the use of omega-3 fatty acids, monounsaturated fatty acids, and the reduction of arachidonic and trans fatty acids should be taken into account in nutritional therapy [38]. A high intake of omega-3 fatty acids can, therefore, not only reduce the incidence of cancer but also reduce cancer-associated symptoms [47][48][49]. ...
The diagnosis and treatment of cancer are associated with impairment at the physical and at psychological level. In addition, side effects are a potentially treatment-limiting factor that may necessitate dose reduction, delay, or even discontinuation of therapy, with negative consequences for outcome and mean survival. Numerous studies have shown that physical activity and sports and exercise therapy programs are not only practicable but also recommendable for oncologic patients during the acute phase and in the aftercare. Furthermore, nutrition plays an important role in all stages of tumor therapy. A timely integration of a nutrition therapy and physical activity in the form of physiotherapy and sports therapy serves to prevent and reduce treatment-associated side effects. Evidence-based recommendations on cancer prevention through nutrition therapy, physical activity, and sports and exercise therapy should be integrated into treatment plans for oncology patients as well as in health care services for the general population. Individual counselling by trained nutrition and exercise specialists may be advisable to receive concrete recommendations on the respective tumor entity or specific side effects. This mini review is based on a selective literature search in the PubMed database and Cochrane Central Register of Controlled Trials on the subjects of healthy diet and physical activity in primary prevention and follow-up about cancer.
... In our MetS mouse model fed a high-fat diet rich in palmitate, switching to a diet that contains the same fat calories from oleate protects the peripheral nerves from palmitate-induced injury (Rumora et al., 2019). In epidemiological studies, plasma monounsaturated fatty acid levels inversely correlate with insulin resistance (Palomer et al., 2018), the MetS (Guo et al., 2017;Tortosa-Caparrós et al., 2017) and Alzheimer's disease (Solfrizzi et al., 2011;Beydoun et al., 2014). The differential effect of oleate versus palmitate on EV production is recapitulated in various cultures, including hepatocytes (Hirsova et al., 2016) and proximal tubular epithelial cells (Cobbs et al., 2019). ...
The metabolic syndrome (MetS) and Alzheimer's disease share several pathological features, including insulin resistance, abnormal protein processing, mitochondrial dysfunction and elevated inflammation and oxidative stress. The MetS constitutes elevated fasting glucose, obesity, dyslipidaemia and hypertension and increases the risk of developing Alzheimer's disease, but the precise mechanism remains elusive. Insulin resistance, which develops from a diet rich in sugars and saturated fatty acids, such as palmitate, is shared by the MetS and Alzheimer's disease. Extracellular vesicles (EVs) are also a point of convergence, with altered dynamics in both the MetS and Alzheimer's disease. However, the role of palmitate‐ and glucose‐induced insulin resistance in the brain and its potential link through EVs to Alzheimer's disease is unknown. We demonstrate that palmitate and high glucose induce insulin resistance and amyloid precursor protein phosphorylation in primary rat embryonic cortical neurons and human cortical stem cells. Palmitate also triggers insulin resistance in oligodendrocytes, the supportive glia of the brain. Palmitate and glucose enhance amyloid precursor protein secretion from cortical neurons via EVs, which induce tau phosphorylation when added to naïve neurons. Additionally, EVs from palmitate‐treated oligodendrocytes enhance insulin resistance in recipient neurons. Overall, our findings suggest a novel theory underlying the increased risk of Alzheimer's disease in MetS mediated by EVs, which spread Alzheimer's pathology and insulin resistance.
... It reinforces the beneficial effects of LCHF diet to the nutritional control of T2D associated with obesity in clinical trials [30]. Omega-3 and omega-9 fatty acids have previously been shown to affect insulin resistance and T2D, besides their anti-inflammatory actions, the ability to inhibit endoplasmic reticulum stress, improve insulin signaling pathway response, and prolong the survival of pancreatic b cells [31,32]. The outstanding recovery of the glycemic response in u-3 and u-9 groups, demonstrates a great unexplored therapeutic potential of the LCHF diet associated with these specific fat sources in combating T2D linked to obesity. ...
... In contrast to FAw3, FAw6 are considered to have pro-inflammatory properties, and thus, maintaining a lower FAw6/FAw3 ratio is crucial for achieving favorable outcomes in ocular pathology [51]. However, studies on healthy adults have demonstrated that increasing intake of AA or LA does not necessarily result in elevated concentrations of several inflammatory markers [52][53][54]. Epidemiological research has even suggested that AA and LA are associated with reduced inflammation [42,55]. Additionally, a study by Fu et al. [56] showed that a diet rich in FAw6 accelerated the maturation process of retinal neurons while inducing increased metabolism to maintain the energy balance of retinal neurons. ...
Polyunsaturated fatty acids (PUFAs) affect several physiological processes, including visual acuity, but their relationship with diabetic retinopathy (DR) remains elusive. The aim of this study was to determine whether PUFAs have a causal effect on DR. PUFAs- (total and omega-3 [FAw3] and omega-6 [FAw6] fatty acids and their ratio) and DR-associated single nucleotide polymorphisms derived from genome-wide association studies; sample sizes were 114,999 for fatty acids and 216,666 for any DR (ADR), background DR (BDR), severe non-proliferative DR (SNPDR), and proliferative DR (PDR). We hypothesized that the intra-body levels of PUFAs have an impact on DR and conducted a two-sample Mendelian randomization (MR) study to assess the causality. Pleiotropy, heterogeneity, and sensitivity analyses were performed to verify result reliability. High levels of PUFAs were found to be associated with reduced risk of both ADR and PDR. Moreover, FAw3 was associated with a decreased risk of PDR, whereas FAw6 demonstrated an association with lowered risks of both BDR and PDR. Our findings provide genetic evidence, for the first time, for a causal relationship between PUFAs and reduced DR risk. Consequently, our comprehensive MR analysis strongly urges further investigation into the precise functions and long-term effects of PUFAs, FAw3, and FAw6 on DR.
... In another study, EPA (100 µM) supplementation for 24 h to 3T3-L1 adipocytes showed increased fatty acid β-oxidation in parallel with a rise in Carnitine Palmitoyltransferase 1A (CPT-1A) activity [88]. In other studies, n-3 PUFAs induced a decrease in body weight and fat mass along with a lowering of triglyceride levels [89][90][91]. Furthermore, some studies also confirmed improvement in glucose or insulin tolerance in models treated with EPA/DHA [92]. ...
... It has been speculated that these fatty acids may induce the expression of inflammatory pathways, including toll-like receptors, protein kinase C, and NOD-like receptors, among others [9]. Polyunsaturated fatty acids (PUFA), specifically the n-6 family, have also been linked to a decrease in pro-inflammatory markers such as IL-6, TNFα, and vascular cell adhesion molecule 1 (VCAM-1) [10]; however, there is some controversy in this regard, as other studies have found the opposite [11]. ...
Previous trials have demonstrated that modifying dietary fat composition can influence the production of inflammation-related factors. Additionally, it has been suggested that not only the type of fat, but also the timing of fat intake can impact these factors. Therefore, the objective of the present study was to evaluate the effect of altering breakfast fat composition on inflammatory parameters. A 3-month crossover randomized trial was designed, involving 60 institutionalized women who alternately consumed a breakfast rich in polyunsaturated fatty acids (PUFA) (margarine), monounsaturated fatty acids (MUFA) (virgin olive oil), or saturated fatty acids (SFA) (butter), based on randomization. The following inflammatory markers were evaluated: epidermal growth factor (EGF), interferon (IFN)-α, interleukin (IL)-1α, IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10, monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor (TNF)-α, C-reactive protein (CRP), and vascular/endothelial growth factor (VEGF). The results showed that the most significant effects were observed with the high-MUFA breakfast, as there was a statistically significant decrease in plasma IL-6 (p = 0.016) and VEGF values (p = 0.035). Other factors, such as IL-1α and CRP, also decreased substantially, but did not reach the statistically significant level. On the other hand, the high-PUFA breakfast induced a significant decrease in EGF levels (p < 0.001), whereas the high-SFA breakfast had no apparent effect on these factors. In conclusion, modifying breakfast fat, particularly by increasing MUFA or PUFA intake, appears to be sufficient for promoting a lower inflammatory marker synthesis profile and may be beneficial in improving cardiovascular complications.
... While the exact mechanism remains unknown, omega-3 PUFAs can reduce the level of key inflammatory cytokines such as tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6). They can also downregulate nuclear factor kappa B (NF-κB), a central mediator in activation of the "nucleotide-binding domain, leucine-richcontaining family, pyrin domain-containing-3" (NLRP3) inflammasome [12][13][14]. ...
Diabetic retinopathy (DR) is a common microvascular complication of type 2 Diabetes Mellitus (T2DM) that can have vision-threatening consequences, particularly if it advances to the proliferative stage and is left untreated. Owing to the central role of hyperglycemia-induced oxidative stress, multiple anti-oxidants have been investigated for their therapeutic value. However, there is a lack of substantial data to support the use of any of the compounds tested so far. Omega-3 polyunsaturated fatty acids (PUFAs), namely docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), have received much acclaim for their positive impact on cardiovascular health outcomes. The anti-oxidative, anti-inflammatory and neuroprotective properties of PUFAs also make them promising therapeutic and preventive agents for DR. The current evidence is derived mainly from in vitro and animal studies and provides some insight into the underlying mechanisms involved. These fatty acids are capable of direct anti-oxidative and anti-inflammatory effects. They also concomitantly promote intrinsic defense mechanisms and recovery, particularly of photoreceptor neurons. Hence, dietary supplementation with PUFAs, mainly from marine sources, can halt and reverse the retinal damage seen in DR. Furthermore, clinical trials have reported improved vision and quality of life in DR patients after supplementation. However, a major limitation of these trials is the use of nutraceutical formulations in which omega-3 PUFAs are combined with other anti-oxidant compounds, thereby preventing the evaluation of omega-3 as standalone treatment. Although the results of experimental studies to date have been promising, more clinical trials are required to determine the full extent of benefits in patients with DR.
... The transcriptome technology was performed to determine the effects of L. plantarum L47 and inulin on ileal mucosa. According to the results of the KEGG enrichment analysis, L. plantarum L47 and inulin relieved ileal inflammation in the ETEC-challenged pigs mainly by affecting LA metabolism and ALA metabolism, products of which have anti-inflammatory properties (Tortosa-Caparros et al., 2017). To validate the transcriptome analysis results, we performed qRT-PCRs to detect the transcription expressions of four DEG (PLA2G2A, PLB1, LOC110259329, and CYP3A29) and their metabolites (AA, LA, ALA, 20-HETE, and 12,13-EpOME). ...
Alternatives to antibiotics for preventing bacteria-induced inflammation in early-weaned farm animals are sorely needed. Our previous study showed that Lactiplantibacillus plantarum L47 and inulin could alleviate dextran sulfate sodium (DSS)-induced colitis in mice. To explore the protective effects of L. plantarum L47 and inulin on the ileal inflammatory response in weaned piglets challenged with enterotoxigenic Escherichia coli (ETEC), 28 weaned piglets were assigned into four groups, namely, CON group-orally given 10 mL/d phosphate buffer saline (PBS), LI47 group-orally given a mixture of 10 mL/d L. plantarum L47 and inulin, ECON group-orally given 10 mL/d PBS and challenged by ETEC, and ELI47 group-orally given 10 mL/d L. plantarum L47 and inulin mixture and challenged by ETEC. The results demonstrated that the combination of L. plantarum L47 and inulin reduced inflammatory responses and relieved the inflammatory damage caused by ETEC, including ileal morphological damage, reduced protein expression of ileal tight junction, decreased antioxidant capacity, and decreased anti-inflammatory factors. Transcriptome analysis revealed that L. plantarum L47 and inulin up-regulated the gene expression of phospholipase A2 group IIA (PLA2G2A) (P < 0.05) as well as affected alpha-linolenic acid (ALA) metabolism and linoleic acid metabolism. Moreover, L. plantarum L47 and inulin increased the levels of ALA (P < 0.05), lipoteichoic acid (LTA) (P < 0.05), and 12,13-epoxyoctadecenoic acid (12,13-EpOME) (P < 0.05) and the protein expression of Toll-like receptor 2 (TLR2) (P = 0.05) in the ileal mucosa. In conclusion, L. plantarum L47 and inulin together alleviated ETEC-induced ileal inflammation in piglets by up-regulating the levels of ALA and 12,13-EpOME via the LTA/TLR2/PLA2G2A pathway.
... The n-3 PUFA:n-6 PUFA ratio is a valuable indicator of the balance between these two types of fatty acids in the body. N-3 PUFA and n-6 PUFA compete for the same enzymes involved in their metabolism and exert opposing effects on inflammatory pathways [66]. A review also discovered that n-3 and n-6 PUFA have opposing effects on the human body [67], implying that n-3 PUFA and n-6 PUFA may have a competitive relationship. ...
Supplemental n-3 polyunsaturated fatty acids (PUFA) on bone metabolism have yielded inconsistent results. This study aimed to examine the effects of n-3 PUFA supplementation on bone metabolism markers and bone mineral density through a meta-analysis of randomized controlled trials. A systematic literature search was conducted using the PubMed, Web of Science, and EBSCO databases, updated to 1 March 2023. The intervention effects were measured as standard mean differences (SMD) and mean differences (MD). Additionally, n-3 PUFA with the untreated control, placebo control, or lower-dose n-3 PUFA supplements were compared, respectively. Further, 19 randomized controlled trials (RCTs) (22 comparisons, n = 2546) showed that n-3 PUFA supplementation significantly increased blood n-3 PUFA (SMD: 2.612; 95% CI: 1.649 to 3.575). However, no significant effects were found on BMD, CTx-1, NTx-1, BAP, serum calcium, 25(OH)D, PTH, CRP, and IL-6. Subgroup analyses showed significant increases in femoral neck BMD in females (0.01, 95% CI: 0.01 to 0.02), people aged 6 months (−0.19, 95% CI: −0.37 to −0.01). The present study demonstrated that n-3 PUFA supplementation might not have a significant effect on bone mineral density or bone metabolism markers, but have some potential benefits for younger postmenopausal subjects in the short term. Therefore, additional high-quality, long-term randomized controlled trials (RCTs) are warranted to fully elucidate the potential benefits of n-3 PUFA supplementation, as well as the combined supplementation of n-3 PUFA, on bone health.
... Omega-3 fatty acids, especially DHA, are likely to treat several diseases. Numerous animal and clinical studies indicated anti-inflammatory properties for DHA (Tortosa-Caparrós et al., 2017;Yates et al., 2014). In this study, the accumulation of IL1β was similar between all doses when DHA from the control group was measured (P >0.05; Figure 2A); in contrast, the collection of IL6 decreased at 200 and 400 μM of DHA (P < 0.05; Figure 2B), on those endometrial explants incubated for 48 h with DHA (control group). ...
Fatty acids are considered metabolic intermediaries, although new facts indicate they also work as signaling molecules with different roles in the immune response. Based on that, in this study, we investigated the anti-inflammatory effects of n-3 polyunsaturated fatty acids (PUFAs) as eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and α-linolenic acid (LNA) in ex vivo bovine endometrial explants. For this, two groups were formed: (1) LPS-challenged and (2) control, both to evaluate the accumulation of proinflammatory cytokines as interleukin 1β (IL1B) and interleukin 6 (IL6). To develop the study, bovine female reproductive tracts from non-pregnant Angus heifers without evidence of reproductive diseases were selected. Endometrial explants were processed and treated for 24 h with EPA, DHA, and LNA in five different concentrations (0μM, 50μM, 100 μM, 200μM and 400 μM) and then, challenged with LPS for 24 h. Supernatants were collected to evaluate the concentration of IL1B and IL6 by ELISA. Explants treated with EPA from control groups reduced the concentrations of ILB (200µM) and IL6 (400 µM), and IL6 (50 µM; 100 µM) from the LPS-challenged group. DHA decreased the accumulation of IL1B and IL6 at 200 µM on explants from the LPS-challenged group, and 200 µM reduced IL6 from the control group. In contrast, explants treated with LNA only reduced the accumulation of IL1B to 400μM (from both groups). In conclusion, the EPA acid is the best anti inflammatory option to decrease the concentration of both pro-inflammatory cytokines (IL1B and IL6) from LPS-challenged and control groups in bovine endometrial explants; while LNA evidence to be the last option to promote an anti-inflammatory response.
... Ancak 30 gün süre ile günlük 0,4g/kg balık yağı takviyesinin yapıldığı bir çalışmada artmış eritrosit katalaz aktivitesinin, serum malondialdehit ve nitrikoksit konsantrasyonlarının azaldığı bulunmuştur (Arnal, et al., 2009). Diyetle ALA alımı serum CRP konsantrasyonu ile ters ilişkili iken, EPA veya DHA alımıile CRP konsantrasyonları arasında bir ilişki görülememiştir (Tortosa-Caparrós, et al., 2017). ...
Özet
Metabolik sendrom, kardiyovasküler morbidite ve mortalitenin artmasına katkıda bulunan abdominal obezite, insülin direnci, bozulmuş açlık glukozu, aterojenik dislipidemi ve hipertansiyon gibi bir dizi metabolik bozukluğun bir arada olduğu kompleks bir hastalıktır. Yetişkin popülasyonda yüksek prevalansa sahip olan metabolik sendrom, küresel hastalık yükünün de önemli bir bileşenidir. Patogenezi net olmamakla birlikte abdominal obezite ve insülin direnci, metabolik sendromun baskın nedensel faktörleri olarak gösterilmektedir. Tedavisi ve yönetimi için ana terapötik stratejiler daha çok beslenme alışkanlıklarının ve fiziksel aktivitenin düzenlenmesine yönelik olsa da metabolik sendromun yönetimi için en etkili diyet modeli henüz kesin olarak belirlenememiştir. Bu nedenle yaşam tarzı değişikliklerinin yanı sıra omega-3 çoklu doymamış yağ asidi, konjuge yağ asitleri, steroller, orta zincirli yağ asitleri, diasilgliseroller ve fosfolipidler gibi fonksiyonel lipitlerin kullanımının, kardiyovasküler hastalık riskini azalttığı bildirilmektedir. Bu biyoaktif lipitlerin potansiyel mekanizması; karaciğer, serum ve abdominal yağ dokusunda lipit birikimini baskılamak, yağ asidi beta-oksidasyonunu artırmak, bağışıklık fonksiyonunu ve doku homeostazını korumak, inflamatuar süreçlerin regülasyonunu sağlamak, termojenezi artırmak, PPARγ aktivasyonu yoluyla adipositokinlerin üretimini düzenlemek, lipit ve glukoz metabolizmasının transkripsiyonel regülasyonunu sağlamaktır. Fonksiyonel lipitlerin günlük beslenmede yer alması ağırlık kaybına, kan basıncı ve kan şekeri regülasyonuna, endotel hasarın önlenmesine/azaltılmasına, lipid profilinin iyileştirilmesine, inflamasyonun ve oksidatif hasarın azaltılmasına katkı sunabilir. Bu etkilerinden dolayı fonksiyonel lipitler metabolik sendrom şiddetinin hafifletilmesinde, komorbiditelerin önlenmesinde ve hastalığın klinik yönetiminde faydalı olabilir.
ABSTRACT
Metabolic syndrome is a complex disease with a combination of metabolic disorders, including abdominal obesity, insulin resistance, impaired fasting glucose, atherogenic dyslipidemia, and hypertension, contributing to increased cardiovascular morbidity and mortality. The metabolic syndrome is highly prevalent in the adult population and is an important component of the global disease burden. Although the pathogenesis is unclear, abdominal obesity and insulin resistance have been implicated as the dominant causal factors of metabolic
... Because humans lack the natural desaturase enzymes necessary for its synthesis, ALA, an essential fatty acid, cannot be produced by the body and must be obtained through diet. ALA is then transformed into the long-chain omega-3 PUFA, EPA, or DHA, in the human body [58]. ...
Insulin resistance is a critical pathophysiological process in the onset and advancement of type 2 diabetes mellitus. It is well-recognized that alterations in the metabolism of lipids and aberrant fat buildup effectively trigger the development of resistance to insulin. Adjusting one’s eating habits and managing weight appropriately are crucial for treating, controlling, and reducing the risk of T2DM because obesity and a lack of physical exercise are the primary factors responsible for the worldwide rise in T2DM. Omega-3 fatty acid is one of the polyunsaturated fatty acids (PUFA)
that include long-chain omega-3 fatty acids such as eicosapentaenoic acid and docosahexaenoic acid,commonly found in fish oils. Omega-3 and omega-6 polyunsaturated fatty acids (PUFAs; 3 and
6 PUFAs) are essential for human health because they serve as metabolic precursors of eicosanoids, a class of signaling molecules that are essential for controlling a body’s inflammation. Since humans are unable to produce any of the omega-3 or omega-6 PUFAs, they both constitute imperative nutritional ingredients. Long-standing concerns about long-chain omega-3 fatty acids’ impact on diabetes
management have been supported by experimental investigations that found significant increases in
fasting glucose following omega-3 fatty acid supplementation and foods rich in PUFA and omega-3 fatty acid. Cellular explanations to explain the connection between inflammation and IR include
mitochondrial dysfunction, endoplasmic reticulum (ER) stress, and oxidative stress. Modifications in the lipid composition of mitochondrial membranes and/or receptor-mediated signaling may be part of the mechanism behind the activation of mitochondrial fusion by fish oil/omega-3 PUFA. The exactmolecular processes by which omega-3 PUFAs control mitochondrial activity to defend against IR are still unknown.
... 3 Several studies have shown that certain types of FAs, particularly docosahexaenoic acid (omega-3), can be converted to anti-inflammatory compounds in vivo, thereby counteracting the effects of pro-inflammatory compounds. 4 On the other hand, inflammatory stimuli can also have an impact on lipid metabolism. Upon exposure to lipopolysaccharide (LPS) and palmitic acid, the TLR4 inflammatory signalling pathway was observed to induce an elevation in sterol regulatory element-binding protein-2-mediated cholesterol accumulation in HepG2 cells. ...
Background
The fundamental initial step in the metabolic process of fatty acids (FA) is facilitated by Acyl‐coenzyme A synthetase (ACS). ACS enables FAs to engage in both anabolic and catabolic pathways by creating thioester bonds with CoA, thus triggering their activation. This paper demonstrated the effect of in vitro cells on the ACS family of key enzymes in FA metabolism in response to inflammatory or lipid stimulating factors and provided insight into the relevant metabolic mechanisms.
Methods
The expression levels of 27 ACS family members were assessed across various lung epithelial cell lines, such as HBE, SPC‐1A, or NCI‐H460, in response to external challenges including lipopolysaccharide (LPS), lysophosphatidylcholine (lysoPC), cigarette smoking extract (CSE), cholesterol, and interference with the ACSL5 gene in response to FASN, CPT1A inhibitors.
Results
Our data showed that ACSF2 was highly expressed in SPC‐A1 and NCI‐H460 cells compared with HBE cell, while ACSL4 and ACSVL4 were lower expressed. The 27 ACS family genes associated with FA metabolism varied under several different exogenous stimuli.
... LA makes up the majority (about 90%) of dietary PUFAs, while AA has a lower intake [257]. In the body, the majority of LA is transformed into AA [258]. For several enzymes, AA serves as a substrate [181]. ...
Abstract Type 2 diabetes mellitus (T2DM), one of the main types of Noncommunicable diseases (NCDs), is a systemic inflammatory disease characterized by dysfunctional pancreatic β-cells and/or peripheral insulin resistance, resulting in impaired glucose and lipid metabolism. Genetic, metabolic, multiple lifestyle, and sociodemographic factors are known as related to high T2DM risk. Dietary lipids and lipid metabolism are significant metabolic modulators in T2DM and T2DM-related complications. Besides, accumulated evidence suggests that altered gut microbiota which plays an important role in the metabolic health of the host contributes significantly to T2DM involving impaired or improved glucose and lipid metabolism. At this point, dietary lipids may affect host physiology and health via interaction with the gut microbiota. Besides, increasing evidence in the literature suggests that lipidomics as novel parameters detected with holistic analytical techniques have important roles in the pathogenesis and progression of T2DM, through various mechanisms of action including gut-brain axis modulation. A better understanding of the roles of some nutrients and lipidomics in T2DM through gut microbiota interactions will help develop new strategies for the prevention and treatment of T2DM. However, this issue has not yet been entirely discussed in the literature. The present review provides up-to-date knowledge on the roles of dietary lipids and lipidomics in gut-brain axis in T2DM and some nutritional strategies in T2DM considering lipids- lipidomics and gut microbiota interactions are given.
... El pescado se debe comer al menos dos veces por semana para la prevención del síndrome metabólico y enfermedad cardiovascular, situación especial que se debe considerar en la dieta, donde los pobladores de la costa son los más beneficiados. (27) Los resultados del trabajo que se realizó difieren del reporte de Torris y otros (28) en el que participantes de 60 a 70 años de edad que consumieron pescado magro una vez a la semana o más, tuvieron un riesgo menor de tener síndrome metabólico en comparación con aquellos que consumieron pescado magro menos de una vez a la semana e inclusive, no se encontró asociación para el consumo de pescado graso en los grupos de edad menor de 45 o 45-59 años, a diferencia del presente estudio. En el caso de los lácteos, ...
Introducción: El síndrome metabólico es una patología compleja que involucra obesidad abdominal, hipertensión, dislipidemias e hiperglicemia.
Objetivo: Determinar los factores alimentarios relacionados con el síndrome metabólico en el personal docente y administrativo de la Escuela de Farmacia y Bioquímica de la Universidad Católica “Los Ángeles de Chimbote”, entre los meses de septiembre a diciembre de 2019.
Métodos: El diseño del estudio fue no experimental, descriptivo correlacional y de corte transversal. Participaron 43 colaboradores quienes respondieron un cuestionario sobre hábitos alimentarios en función al consumo de snacks, bebidas azucaradas industrializadas, galletas, carnes rojas, pescado y cereales. Se identificó la presencia del síndrome metabólico a través del empleo de los criterios de la Asociación Latinoamericana de Diabetes. A su vez, las determinaciones de glucosa y el perfil lipídico se determinaron con el uso de glucómetro Accu Chek Performa Nano y Colesterómetro Missión 3 en 1. Para el análisis estadístico se utilizó la prueba de contingencia de la ji al cuadrado. El estudio se realizó con personal de la Escuela de Farmacia y Bioquímica de la Universidad Católica “Los Ángeles de Chimbote”, Perú., entre los meses de septiembre a diciembre de 2019.
Resultados: Se determinó en los colaboradores un consumo inadecuado de frutas en el 83,7 % de los colaboradores; cereales en el 69,8 %; leche sin grasa en el 55,8 %; pescado en el 46,5 %; leche con grasa en el 37,2 % y bebidas azucaradas en el 34,9 %. Por otra parte, los participantes presentaron los siguientes porcentajes de padecimiento: el 44,19 % síndrome metabólico, el 72,09 % un índice aterogénico elevado; el 65,12 % prediabetes, el 48,84 % hipertrigliceridemia y el 51,16 % obesidad abdominal.
Conclusiones: El consumo de bebidas azucaradas y el bajo consumo de pescado constituyeron factores alimentarios que se asociaron con el síndrome metabólico.
... Another interesting anti-inflammatory approach includes nutritional interventions with omega-3 polyunsaturated fatty acids (n-3 PUFA), such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). These n-3 fatty acids are found in oily fish and fish oil supplements, and exert diverse anti-inflammatory effects, attractive for patients with coronary artery disease [81]. EPA and DHA act on many steps of coronary atherosclerosis; n-3 PUFA can reduce the expression of adhesion molecules on endothelial cells, inhibit leukocyte-endothelial cell adhesion, and reduce the production of inflammatory cytokines [82]. ...
Inflammation plays an important role in all stages of atherosclerosis — from endothelial dysfunction, to formation of fatty streaks and atherosclerotic plaque, and its progression to serious complications, such as atherosclerotic plaque rupture. Although dyslipidemia is a key driver of atherosclerosis, pathogenesis of atherosclerosis is now considered interplay between cholesterol and inflammation, with the significant role of the immune system and immune cells. Despite modern therapeutic approaches in primary and secondary cardiovascular prevention, cardiovascular diseases remain the leading cause of mortality worldwide. In order to reduce residual cardiovascular risk, despite the guidelines-guided optimal medical therapy, novel therapeutic strategies are needed for prevention and management of coronary artery disease. One of the innovative and promising approaches in atherosclerotic cardiovascular disease might be inflammation-targeted therapy. Numerous experimental and clinical studies are seeking into metabolic pathways underlying atherosclerosis, in order to find the most suitable pathway and inflammatory marker/s that should be the target for anti-inflammatory therapy. Many anti-inflammatory drugs have been tested, from the well-known broad range anti-inflammatory agents, such as colchicine, allopurinol and methotrexate, to targeted monoclonal antibodies specifically inhibiting a molecule included in inflammatory pathway, such as canakinumab and tocilizumab. To date, there are no approved anti-inflammatory agents specifically indicated for silencing inflammation in patients with coronary artery disease. The most promising results came from the studies which tested colchicine, and studies where the inflammatory-target was NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome/interleukin-1 beta (IL-1β)/interleukin-6 (IL-6)/C-reactive protein (CRP) pathway. A growing body of evidence, along with the ongoing clinical studies, suggest that the anti-inflammatory therapy might become an additional strategy in treating atherosclerotic cardiovascular disease. Herein we present an overview of the role of inflammation in atherosclerosis, the most important inflammatory markers chosen as targets of anti-inflammatory therapy, along with the critical review of the major clinical trials which tested non-targeted and targeted anti-inflammatory drugs in patients with atherosclerotic cardiovascular disease.
... Fatty acids are oxidized in the mitochondria as the primary energy source in the healthy heart. In addition, these two 18-chain fatty acids are precursors to arachidonic acid (20:4, omega-6) and eicosapentaenoic acid (20:5, omega-3) which are substrates for pro-inflammatory and anti-inflammatory mediators, respectively 37,38 . In general, enriched pathways that were different between all dogs with DCM vs. healthy controls were amino acid-related whereas enriched pathways in the DCM-NT vs. DCM-T comparison were lipid-related. ...
Dilated cardiomyopathy (DCM), caused by genetic and environmental factors, usually progresses to heart failure, a major cause of death in elderly people. A diet-associated form of DCM was recently identified in pet dogs eating non-traditional (NT) diets. To identify potential dietary causes, we analyzed metabolomic signatures and gene set/pathway enrichment in (1) all dogs based on disease, diet, and their interactions and (2) dogs with DCM based on diet. Metabolomic analysis was performed in 38 dogs with DCM eating NT diets (DCM-NT), 8 dogs with DCM eating traditional diets, 12 healthy controls eating NT diets, and 17 healthy controls eating traditional diets. Overall, 153 and 63 metabolites differed significantly between dogs with DCM versus healthy controls and dogs eating NT versus traditional diets, respectively, with 12 metabolites overlapping both analyses. Protein–protein interaction networks and gene set enrichment analysis identified 105 significant pathways and gene sets including aging-related pathways (e.g., nuclear factor-kappa B, oxidative damage, inflammation). Seventeen metabolites differed significantly in dogs with DCM eating NT versus traditional diets (e.g., fatty acids, amino acids, legume biomarkers), suggesting different mechanisms for primary versus diet-associated DCM. Our multifaceted metabolomic assessment of DCM in dogs highlighted diet’s role in some forms of DCM.
... 1 It has been demonstrated that n-3 and n-6 FAs modulate the production of inflammatory signaling molecules and are thus involved in anti-inflammatory processes and autoimmune-related diseases. 2,3 Multiple studies have also shown the promising health benefits of n-3 FAs from sea fish with lowering the risk of cardiovascular disease (CVD), age-associated cognitive decline, and Alzheimer's disease. 1,4 However, many epidemiological studies and meta-analyses have generated neutral or conflicting evidence that there were weak, or even inverse, associations between n-3 FA intake from fish oil supplements and the risk of a wide range of human diseases, including cardiovascular diseases (CVD) and stroke, 5,6 cancers, 6 and type 2 diabetes (T2DM). ...
Omega-3 polyunsaturated fatty acids (n-3 FAs) are essential nutrients and are considered effective in improving human health. Recent studies highlight the importance of the combination of n-3 FAs and polyphenols for limiting the oxidation of n-3 FAs and exhibiting synergistic beneficial effects. Herein, we developed a novel formulation technology to prepare oleogels that could be used for the codelivery of n-3 FAs and polyphenols with high loading efficacy and oxidative stability. These oleogels are made from algal oil with polyphenol-enriched whey protein microgel (WPM) particles as gelling agents via simple and scalable ball milling technology. The oxidative status, fatty acid composition, and volatiles of protein oleogels during accelerated storage were systematically assessed by stoichiometry and gas chromatography-mass spectrometry. These results showed that protein oleogels could overcome several challenges associated with the formulation of n-3 oils, including long-term oxidative stability and improved sensory and textural properties. The protein oleogel system could provide an excellent convenience for formulating multiple nutrients and nutraceuticals with integrating health effects, which are expected to be used in the care of highly vulnerable populations, including children, the elderly, and patients.
... B. ovatus is inversely associated with BMI (34), and B. vulgatus has been found to protect against coronary artery disease (35). In addition, dietary diversity was positively associated with fecal n-3 PUFAs, which are known anti-inflammatory substrates and help prevent chronic diseases, including cardiovascular disease and T2D (36). ...
Background
Dietary diversity is essential for human health. The gut ecosystem provides a potential link between dietary diversity, host metabolism, and health, yet this mechanism is poorly understood.
Objectives
Here, we aimed to investigate the relation between dietary diversity and the gut environment as well as host metabolism from a multiomics perspective.
Methods
Two independent longitudinal Chinese cohorts (a discovery and a validation cohort) were included in the present study. Dietary diversity was evaluated with FFQs. In the discovery cohort (n = 1916), we performed shotgun metagenomic and 16S ribosomal ribonucleic acid (rRNA) sequencing to profile the gut microbiome. We used targeted metabolomics to quantify fecal and serum metabolites. The associations between dietary diversity and the microbial composition were replicated in the validation cohort (n = 1320).
Results
Dietary diversity was positively associated with α diversity of the gut microbiota. We identified dietary diversity–related gut environment features, including the microbial structure (β diversity), 68 microbial genera, 18 microbial species, 8 functional pathways, and 13 fecal metabolites. We further found 332 associations of dietary diversity and related gut environment features with circulating metabolites. Both the dietary diversity and diversity-related features were inversely correlated with 4 circulating secondary bile acids. Moreover, 16 mediation associations were observed among dietary diversity, diversity-related features, and the 4 secondary bile acids.
Conclusions
These results suggest that high dietary diversity is associated with the gut microbial environment. The identified key microbes and metabolites may serve as hypotheses to test for preventing metabolic diseases.
... The evidence regarding linoleic acid with obesity and insulin resistance is conflicting. While some observational and metabolomic studies show inverse associations between obesity and insulin resistance others show the converse [22,[48][49][50][51]. Likewise, mechanistically, evidence is equivocal on whether linoleic acid promotes or protects against insulin resistance. ...
High carbohydrate, lower fat (HCLF) diets are recommended to reduce cardiometabolic disease (CMD) but low carbohydrate high fat (LCHF) diets can be just as effective. The effect of LCHF on novel insulin resistance biomarkers and the metabolome has not been fully explored. The aim of this study was to investigate the impact of an ad libitum 8-week LCHF diet compared with a HCLF diet on CMD markers, the metabolome, and insulin resistance markers. n = 16 adults were randomly assigned to either LCHF (n = 8, <50 g CHO p/day) or HCLF diet (n = 8) for 8 weeks. At weeks 0, 4 and 8, participants provided fasted blood samples, measures of body composition, blood pressure and dietary intake. Samples were analysed for markers of cardiometabolic disease and underwent non-targeted metabolomic profiling. Both a LCHF and HCLF diet significantly (p < 0.01) improved fasting insulin, HOMA IR, rQUICKI and leptin/adiponectin ratio (p < 0.05) levels. Metabolomic profiling detected 3489 metabolites with 78 metabolites being differentially regulated, for example, an upregulation in lipid metabolites following the LCHF diet may indicate an increase in lipid transport and oxidation, improving insulin sensitivity. In conclusion, both diets may reduce type 2 diabetes risk albeit, a LCHF diet may enhance insulin sensitivity by increasing lipid oxidation.
... There have been many studies that examined and confirmed the correlation of n-3 and n-6 FAs to various chronic illnesses such as hypertension and obesity [3][4][5][6][7]. Both n-3 and n-6 FAs provide protective effects for chronic inflammatory diseases such as obesity, diabetes, and metabolic syndrome [8,9]. In addition, it has been reported that these FAs have a correlation to parameters that are related to glucose metabolism such as insulin and HbA1c in metabolic syndrome [10]. ...
Background and Objectives: The relation of dietary n-6 fatty acid to metabolic syndrome has not been examined and clearly defined. To improve health in the general population, this study was to investigate the role of n-3 and n-6 fatty acids in the reduction in metabolic syndrome and to observe changes in the effects of these fatty acids depending on the level of insulin resistance. Materials and Methods: This cross-sectional study utilized national health and nutrition survey data from 2014 to 2016. From the data, a relation of n-3 and n-6 fatty acid intakes to metabolic syndrome and Hemoglobin A1c (HbA1c)’s role in the relation was evaluated and analyzed for 4852 patients between 40 and 64 years old. Intake frequency of 112 nutrition and daily consumption amounts were identified, and intakes of n-3 and n-4 fatty acids were calculated from this data. Metabolic syndrome was determined for each participant using diagnostic standards for the Asian population published by the National Cholesterol Education Program. Results: Among the total 4852 subjects, 1583 (32.6%) had metabolic syndrome; 736 of 1875 (39.3%) males and 847 of 2977 (28.5%) females had the syndrome. In males, when their HbA1c was low (<5.4%), intakes of both n-3 and n-6 fatty acids were related to a 43–63% decreased prevalence of metabolic syndrome with significance, and a similar negative tendency was also observed in females. On the contrary, for both males and females, no statistically significant correlation was present when HbA1c was high. Conclusion: It was considered that consistent and regular dietary intakes of n-3 and n-6 fatty acids may contribute greatly to prevent or treat metabolic syndrome in healthy males with normal insulin sensitivity, but the effect of their dietary intakes was found to be limited in a group with strong insulin resistance. The conclusion of this study presents a valuable reference and knowledge to provide nutritional education to the general population.
... Food sources high in PUFAs present two opposite effects in humans, namely, promotion of beneficial effects due to anti-inflammatory properties of PUFA and contribution to oxidative stress through exposure to hazardous substances as a result of PUFAs degradation through oxidation processes (10,11). Actually, there are several mitigation strategies to minimize oxidation processes along the food chain (12)(13)(14), but the physiological oxidative processes that take place during gastrointestinal digestion will happen despite the presence of those antioxidant agents (15,16). ...
Meat and fish are introduced into the diet as a source of protein, but these muscle foods present different fatty acid (FA) compositions and different lipid stabilities. Fatty fish is expected to oxidize due to its higher content of polyunsaturated FA (PUFA), whereas the higher heme-Fe content of red meat will also affect lipid stability. Combining other food ingredients within a meal also influences lipid oxidation, which will not stop after meals intake. This is due to the acidic environment of the stomach together with the presence of metallic ions, a process that is scarcely understood. The goal of this study was to evaluate the oxidation of fatty fish vs. meat meal diets under in vitro standardized semi-dynamic gastric conditions and FA release from the stomach to the duodenum. Meal diets composed by 25% beef meal (BM) or fatty fish meal (FM), 25% fried potatoes, and 50% sugar soft drink were prepared. Proximate composition, FA and amino acid profiles, and meals quality indices were evaluated. Their differences in composition led to different total gastric digestion time of 242.74 (BM) and 175.20 (FM) minutes. Using the INFOGEST semi-dynamic gastric model, 4 gastric emptying (GE) were simulated in both meals. In each GE, FA profile and lipid oxidation products (LOPs) formation were assessed. As a result, more than 50% FA release to the duodenum occurred in GE1, whose percentage decreased with the time of digestion. FM exhibited the highest LOPs formation, which corroborates the high peroxidizability index measured for this meal diet. Higher LOPs formation occurred in the later GEs, which released less FA. This suggests that higher times of residence in the stomach increase FA oxidation. This study shows a higher formation of LOPs during digestion of FM using a whole meal approach. These results relate to its richness in PUFAs compared to BM. Despite higher LOPs formation, FM digests that reached duodenum still contain higher content of unoxidized PUFAs compared with BM and a desirable ω3/ω6 PUFAs ratio of ∼0.43. LOPs formation in PUFA-rich meals could be reduced if those meals have a low caloric value, avoiding large times of residence in the stomach and consequently high levels of oxidation.
... Balancing the ratio of n-6/n-3 PUFAs is strongly recommended for the normal functioning of various physiological processes. The optimal n-6/n-3 PUFA ratio should be approximately 1-2:1 for normal physiological functions in the body due to the competitiveness of n-6 and n-3 PUFAs [30,31]. ALA and linoleic acid (LA) are metabolized by competitive common enzymatic reactions; therefore, increasing the n-6 PUFA consumption by LA intake may inhibit eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) synthesis from n-3 PUFAs. ...
Obesity is closely associated with low-grade chronic and systemic inflammation and dyslipidemia, and the consumption of omega-3 polyunsaturated fatty acids (n-3 PUFAs) may modulate obesity-related disorders, such as inflammation and dyslipidemia. An emerging research question is to understand the dietary intervention strategy that is more important regarding n-3 PUFA consumption: (1) a lower ratio of n-6/n-3 PUFAs or (2) a higher amount of n-3 PUFAs consumption. To understand the desirable dietary intervention method of n-3 PUFAs consumption, we replaced lard from the experimental diets with either perilla oil (PO) or corn oil (CO) to have identical n-3 amounts in the experimental diets. PO had a lower n-6/n-3 ratio, whereas CO contained higher amounts of PUFAs; it inherently contained relatively lower n-3 but higher n-6 PUFAs than PO. After the 12-week dietary intervention in ob/ob mice, dyslipidemia was observed in the normal chow and CO-fed ob/ob mice; however, PO feeding increased the high density lipoprotein-cholesterol (HDL-C) level; further, not only did the HDL-C level increase, the low density lipoprotein-cholesterol (LDL-C) and triglyceride (TG) levels also decreased significantly after lipopolysaccharide (LPS) injection. Consequently, extra TG accumulated in the liver and white adipose tissue (WAT) of normal chow- or CO-fed ob/ob mice after LPS injection; however, PO consumption decreased serum TG accumulation in the liver and WAT. PUFAs replacement attenuated systemic inflammation induced by LPS injection by increasing anti-inflammatory cytokines but inhibiting pro-inflammatory cytokine production in the serum and WAT. PO further decreased hepatic inflammation and fibrosis in comparison with the ND and CO. Hepatic functional biomarkers (aspartate aminotransferase (AST) and alanine transaminase (ALT) levels) were also remarkably decreased in the PO group. In LPS-challenged ob/ob mice, PO and CO decreased adipocyte size and adipokine secretion, with a reduction in phosphorylation of MAPKs compared to the ND group. In addition, LPS-inducible endoplasmic reticulum (ER) and oxidative stress decreased with consumption of PUFAs. Taken together, PUFAs from PO and CO play a role in regulating obesity-related disorders. Moreover, PO, which possesses a lower ratio of n-6/n-3 PUFAs, remarkably alleviated metabolic dysfunction in LPS-induced ob/ob mice. Therefore, an interventional trial considering the ratio of n-6/n-3 PUFAs may be desirable for modulating metabolic complications, such as inflammatory responses and ER stress in the circulation, liver, and/or WAT.
... Se encontró que los contenidos de ácidos grasos tienen efectos tanto peligrosos como benéficos para la salud humana según el tipo de grasas y el consumo de carne (4) . Además, la preocupación de los consumidores por alimentos altos en omega-3 (AGPI ω-3) en su dieta diaria aumentó debido a su efecto benéfico en la salud humana (5,6,7) . ...
The purpose of the study was to assess the effect of the grapeseed meal, added to slow-growing Hubbard broilers diet high in polyunsaturated fatty acids (PUFA) due to the dietary flaxseed meal. The 7-wk feeding trial used 80 broiler chicks (14 d), assigned to two groups: control (C) and E, with 4 replicates of 10 chicks/group. The basal diet was similar for both groups during both feeding stages. The diet for group E was supplemented with 3% grapeseed meal. Six broilers from each group were slaughtered in the end of the feeding trial, and blood, breast and leg meat samples were collected. Serum cholesterol was significantly lower in group E (110.85 mg/dL), than in group C (146.82 mg/dL). The PUFA concentration was significantly higher in group E, than in group C, both in the breast (31.34 %, compared to 27.73 % total fatty acid methyl ester - FAME) and in the leg (32.44 %, compared to 30.06 % total FAME). The cholesterol concentration was significantly lower in group E (42.52 mg), than in group C (60.91 mg/100 g fresh sample) in the leg. After 7 d of refrigeration, the peroxide value was significantly lower in group E (8.11 meq), than in group C (8.79 meq/kg fat) in the breast meat, while fat acidity was significantly lower in group E (40.82 mg KOH), than in group C (43.99 mg KOH / g fat) in the leg. The dietary 3 % grapeseed meal, used as natural antioxidant, in PUFA-enriched broiler diets, had positive effects on the blood parameters and meat quality.
... Diseases or disorders Reference Inflammatory -autoimmune diseases or disorders Cardiovascular risk, diabetes, obesity, metabolic syndrome [29] Cancer [30,31] Neurodegenerative diseases [27] Allergies [32] Asthma [33] Arthritis [34] Hypertension [35] Maternal and child health Infant growth and neurodevelopment [36] Gestational diabetes mellitus [37] primary producer. [40,41] Phytoplankton is mostly consumed by zooplankton or benthic invertebrates such as shellfish, which are, in turn, accumulated at progressively higher trophic levels through the food chain to finalize in humans (Fig. 2). ...
Lipids from marine organisms are a source of molecules of high nutritional significance, like polyunsaturated fatty acids (PUFAs) and antioxidants. The incorporation of these molecules into the human body is possible mainly through the intake of fish and fish oil-based food. This review covers some of the health benefits and biochemical aspects of nutritional lipids, the available marine resources for the production of PUFAs and antioxidants, and the most used methods for the extraction and identification of these natural lipid molecules in the lab and in the industry. Emphasis is put on the use of residual biomass from fisheries to obtain these interesting products and the consequent improvement of the sustainability of the fish industry.
Вступ. За умов метаболічного синдрому порушується функція підшлункової залози, тому важливими є панкреапротекторні властивості лікарських засобів, які використовують для лікування цього стану. Мета дослідження – вивчити вплив полівітамінного комплексу (Aevit premium виробництва АТ “Київський вітамінний завод”), який широко використовують у клінічній практиці, на структуру тканини підшлункової залози сирійських хом’яків за умов експериментального метаболічного синдрому, індукованого кафе-дієтою. Методи дослідження. Метаболічний синдром у сирійських золотавих хом’яків спричиняла кафе-дієта, складовою якої була суміш з промислово оброблених харчових продуктів із вмістом жирів не менше 40 %. Приготовлену суміш давали тваринам з надлишком упродовж 7 тижнів (49 днів). Питну воду було замінено на 10 % розчин фруктози. Досліджуваний полівітамінний комплекс (у дозі 25,8 мг/кг) та препарати порівняння – метформін (у дозі 60,0 мг/кг) і вітамін Е (у дозі 100,0 мг/кг) застосовували, починаючи з 5-го тижня моделювання метаболічного синдрому, протягом 3 тижнів (21 день). Мікропрепарати підшлункової залози виготовляли за загальноприйнятими гістологічними методиками. Переглядали мікропрепарати під світловим мікроскопом Granum L 30 (03), фотографували мікроскопічні зображення цифровою відеокамерою Granum DСМ 310, обробляли фотознімки на комп’ютері Pentium 2,4GHz за допомогою програми Toup View. Результати й обговорення. Після споживання впродовж 7 тижнів кафе-дієти у підшлунковій залозі сирійських хом’яків виявлено певні ознаки виснаженості інсулярного апарату: зниження “якості” частини бета-клітин у панкреатичних острівцях, зменшення чисельності цих клітин, збільшення відносної частки дуже дрібних та дрібних і зменшення частки середніх панкреатичних острівців. Під впливом полівітамінного комплексу чисельність панкреатичних острівців, відсотковий розподіл їх за класами показово перевищували аналогічні показники у тварин контрольної патології і практично відповідали інтактному контролю. Висновки. Досліджуваний полівітамінний комплекс сприяє зменшенню напруження інсуліноцитів та панкреацитів підшлункової залози у сирійських хом’яків з моделлю метаболічного синдрому. Встановлено, що за виразністю коригувального впливу на стан підшлункової залози хом’яків із метаболічним синдромом полівітамінний комплекс не поступається препаратам порівняння – вітаміну Е і метформіну.
Objective
To systematically assess the efficacy of ω-3 polyunsaturated fatty acids (PUFAs) when treating polycystic ovary syndrome (PCOS).
Methods
This meta-analysis follows Preferred Reporting Items for Systematic Reviews and Meta-Analyses criteria. We searched PubMed, EMBASE, ScienceDirect, Cochrane Library, China journal full-text database, VIP full-text Database, Wanfang Database, and Chinese Biomedical Literature Data for clinical trials on ω-3 PUFAs’ efficacy in treating PCOS. Two independent reviewers examined and analyzed studies, resolving inconsistencies through discussion. RevMan5.3 software performed heterogeneity-based fixed and random-effects meta-analysis. We assessed bias using the Cochrane bias risk assessment tool.
Results
Our meta-analysis included 7 clinical control studies comprising 574 samples to evaluate the impact of ω-3 PUFAs on various metabolic markers in PCOS patients. We observed a significant reduction in total cholesterol (TC) and triglyceride (TG) levels ( P < .05), along with a decrease in insulin resistance as measured by the Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) ( P < .05). Testosterone (T) levels were also lowered in the study group post-treatment ( P < .05). However, no notable effects were found on body mass index (BMI), fasting blood sugar (FBS), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and Ferriman-Gallwey (mFG) scores ( P > .05). Publication bias was not detected, enhancing the robustness of our results. Our study suggests that ω-3 PUFAs could be beneficial in managing specific metabolic markers in PCOS, although the results showed marked heterogeneity.
Conclusion
In PCOS patients, PUFAs can enhance reproductive endocrine, glucose, and lipid levels. However, additional research and extended follow-up are required to confirm this.
Introduction: 9-PAHSA belongs to a class of endogenous mammalian bioactive lipids, fatty acid esters of hydroxy fatty acids (FAHFA), that are present in circulation at nanomolar concentrations in mice and humans. Published preclinical data suggest beneficial effects of 9-PAHSA treatment on glucose metabolism as well as modulation of immune function. However, receptor molecules with high affinity towards these lipids have not been identified so far.
Methods: In a broad screen of a panel of G protein-coupled receptors (GPCRs) we discovered that 9-PAHSA displays antagonist activity with an IC 50 in the micromolar range on selected chemokine receptors, namely, CCR6, CCR7, CXCR4, and CXCR5. The potential immunomodulatory activities in a human cellular model of innate immunity were then investigated.
Results and discussion: In our in vitro experiments, a weak anti-inflammatory potential for high concentrations of 9-PAHSA (10–100 µM) could be detected, as treatment reduced the LPS-induced secretion of certain chemokines, such as CXCL10, MIP-1 beta and MCP. Regarding metabolic effects, we re-investigated 9-PAHSA on glucose metabolism and insulin sensitivity in vitro and in mice confirming conclusions from our earlier study that FAHFAs lack glucoregulatory activity following an acute treatment. In conclusion, the specific interactions with a subset of chemokine receptors may contribute to weak anti-inflammatory properties of 9-PAHSA, but further studies are needed to confirm its in anti-inflammatory potential in vivo .
Background
New statistical methodologies were developed in the last decade to face the challenges of estimating the effects of exposure to multiple chemicals. Weighted Quantile Sum (WQS) regression is a recent statistical method that allows estimating a mixture effect associated with a specific health effect and identifying the components that characterize the mixture effect.
Objectives
In this study, we propose an extension of WQS regression that estimates two mixture effects of chemicals on a health outcome in the same model through the inclusion of two indices, one in the positive direction and one in the negative direction, with the introduction of a penalization term.
Methods
To evaluate the performance of this new model we performed both a simulation study and a real case study where we assessed the effects of nutrients on obesity among adults using the National Health and Nutrition Examination Survey (NHANES) data.
Results
The method showed good performance in estimating both the regression parameter and the weights associated with the single elements when the penalized term was set equal to the magnitude of the Akaike information criterion of the unpenalized WQS regression. The two indices further helped to give a better estimate of the parameters [Positive direction Median Error (PME): 0.022; Negative direction Median Error (NME): −0.044] compared to the standard WQS without the penalization term (PME: −0.227; NME: 0.215). In the case study, WQS with two indices was able to find a significant effect of nutrients on obesity in both directions identifying sodium and magnesium as the main actors in the positive and negative association, respectively.
Discussion
Through this work, we introduced an extension of WQS regression that improved the accuracy of the parameter estimates when considering a mixture of elements that can have both a protective and a harmful effect on the outcome; and the advantage of adding a penalization term when estimating the weights.
The rapid rise in atopy and asthma in industrialized nations has led to the identification of early life environmental factors that promote these conditions and spurred research into how such exposures may mediate the trajectory to childhood disease development. Over the past decade, the human microbiome has emerged as a key determinant of human health. This is largely due to the increasing appreciation for the myriad of non-mutually exclusive mechanisms by which microbes tune and train host immunity. Microbiomes, particularly those in early life, are shaped by extrinsic and intrinsic factors, including many of the exposures known to influence allergy and asthma risk. This has led to the over-arching hypothesis that such exposures mediate their effect on childhood atopy and asthma by altering the functions and metabolic productivity of microbiomes that shape immune function during this critical developmental period. The capacity to study microbiomes at the genetic and molecular level in humans from the pre-natal period into childhood with well-defined clinical outcomes, offers an unprecedented opportunity to identify early-life and inter-generational determinants of atopy and asthma outcomes. Moreover, such studies provide an integrative microbiome research framework that can be applied to other chronic inflammatory conditions. This review attempts to capture key studies in the field that offer insights into the developmental origins of childhood atopy and asthma, providing novel insights into microbial mediators of maladaptive immunity and chronic inflammatory disease in childhood.
Nutraceuticals claim physiological benefits, i.e., why they are called
alternatives to pharmaceuticals. They are formulated from active
components isolated either from plant sources (phytocomplexes) like
herbs or from animal origin like fish, which, when concentrated and
dispensed in an appropriate pharmaceutical form could prevent or treat
certain pathological conditions. Further, nutraceutical may cover a wide
spectrum of commodities such as isolated nutrients, botanicals, dietary
supplements, functional foods, and health supplements. The
nutraceutical market is going to upsurge in the coming years due to the requirement of the public, which transformed from a "want" for
preventive health into a "need" in the current scenario. Thus, it integrates
into the economic growth strategy of any country.
Additionally, end-users, peculiarly those who belong to higher
socio-economic and upper-middle-class sections, perceive nutraceuticals
as a proactive medicine to repress the pre-clinical health conditions.
Therefore, they could be a potential toolkit to be used 'beyond the diet
but before the drugs' to impede or cure the emerging infectious and non�infectious diseases. There is enormous demand for nutraceutical-type
products by the general public in the current market due to their natural
origin, minimal adverse effects, and their wide availability over the
counter in supermarkets, pharmacies, or health product retailers.
Henceforth, safe and biologically available nutraceuticals may work as
pharmaceutical products for the treatment of many diseases and also
improve the physiological functions of the body.
Introduction:
This study aimed to assess the effects of supplementing chicken feed with Moringa oleifera leaf powder, a phytobiotic, on the gastrointestinal microbiota. The objective was to examine the microbial changes induced by the supplementation.
Methods:
A total of 40, one-day-old chickens were fed their basal diet for 42 days and then divided into two groups: SG1 (basal diet) and SG2 (basal diet + 10 g/kg Moringa oleifera leaf powder). Metagenomics analysis was conducted to analyze operational taxonomic units (OTUs), species annotation, and biodiversity. Additionally, 16S rRNA sequencing was performed for molecular characterization of isolated gut bacteria, identified as Enterococcus faecium. The isolated bacteria were tested for essential metabolites, demonstrating antibacterial, antioxidant, and anticancer activities.
Results and discussion:
The analysis revealed variations in the microbial composition between the control group (SG1) and the M. oleifera-treated group (SG2). SG2 showed a 47% increase in Bacteroides and a 30% decrease in Firmicutes, Proteobacteria, Actinobacteria, and Tenericutes compared to SG1. TM7 bacteria were observed exclusively in the M. oleifera-treated group. These findings suggest that Moringa oleifera leaf powder acts as a modulator that enhances chicken gut microbiota, promoting the colonization of beneficial bacteria. PICRUSt analysis supported these findings, showing increased carbohydrate and lipid metabolism in the M.oleifera-treated gut microbiota.
Conclusion:
This study indicates that supplementing chicken feed with Moringa oleifera leaf powder as a phytobiotic enhances the gut microbiota in chicken models, potentially improving overall health. The observed changes in bacterial composition, increased presence of Bacteroides, and exclusive presence of TM7 bacteria suggest a positive modulation of microbial balance. The essential metabolites from isolated Enterococcus faecium bacteria further support the potential benefits of Moringa oleifera supplementation.
Background and objective:
Gestational diabetes mellitus (GDM) "programs" an elevated risk of metabolic dysfunctional disorders in the offspring, and has been associated with elevated leptin and decreased adiponectin levels in cord blood. We sought to assess whether docosahexaenoic acid (DHA) supplementation in GDM affects neonatal metabolic health biomarkers especially leptin and adiponectin.
Methods:
In a randomized controlled trial, singleton pregnant women with de novo diagnosis of GDM at 24-28 weeks of gestation were randomized to dietary supplementation of 500 mg DHA per day (intervention, n = 30) until delivery or standard care (control, n = 38). The primary outcomes were cord blood leptin and total adiponectin concentrations. Secondary outcomes included high-molecular-weight (HMW) adiponectin and insulin-like growth factor-1 (IGF-1) concentrations in cord blood, maternal glycemic control post-intervention and birth weight (z score). In parallel, 38 euglycemic pregnant women were recruited for comparisons of cord blood biomarkers.
Results:
There were no significant differences in cord serum leptin, total and HMW adiponectin and IGF-1 concentrations between DHA supplementation and control groups (all p > 0.05). Maternal fasting and 2-h postprandial blood glucose levels at 12-16 weeks post-intervention were similar between the two groups. The newborns in the DHA group had higher birth weight z scores (p = 0.02). Cord blood total and HMW adiponectin concentrations were significantly lower in GDM vs. euglycemic pregnancies.
Conclusion:
Docosahexaenoic acid supplementation at 500 mg/day in GDM women did not affect neonatal metabolic biomarkers including leptin, adiponectin and IGF-1. The results are reassuring in light of the absence of influence on neonatal adipokines (leptin and adiponectin), and potential benefits to fetal growth and development.
Clinical trial registration:
Clinicaltrials.gov, NCT03569501.
Cardiac aging is evident by a reduction in function which subsequently contributes to heart failure. The metabolic microenvironment has been identified as a hallmark of malignancy, but recent studies have shed light on its role in cardiovascular diseases (CVDs). Various metabolic pathways in cardiomyocytes and noncardiomyocytes determine cellular senescence in the aging heart. Metabolic alteration is a common process throughout cardiac degeneration. Importantly, the involvement of cellular senescence in cardiac injuries, including heart failure and myocardial ischemia and infarction, has been reported. However, metabolic complexity among human aging hearts hinders the development of strategies that targets metabolic susceptibility. Advances over the past decade have linked cellular senescence and function with their metabolic reprogramming pathway in cardiac aging, including autophagy, oxidative stress, epigenetic modifications, chronic inflammation, and myocyte systolic phenotype regulation. In addition, metabolic status is involved in crucial aspects of myocardial biology, from fibrosis to hypertrophy and chronic inflammation. However, further elucidation of the metabolism involvement in cardiac degeneration is still needed. Thus, deciphering the mechanisms underlying how metabolic reprogramming impacts cardiac aging is thought to contribute to the novel interventions to protect or even restore cardiac function in aging hearts. Here, we summarize emerging concepts about metabolic landscapes of cardiac aging, with specific focuses on why metabolic profile alters during cardiac degeneration and how we could utilize the current knowledge to improve the management of cardiac aging.
Endometriosis has been described by many different theories of pathogenesis over the years. It is now also appreciated to be a state of chronic inflammation, and the role of immune dysfunction in its development has been proven. There is increasing evidence to support the role of the microbiome in the formation and progression of endometriosis via inflammatory pathways. The dysbiosis seen in endometriosis is thought to be both causative and a consequence of the pathogenesis. Gut, peritoneal fluid and female reproductive tract microbiota has been studied to understand if there are any microbiome signatures specific to endometriosis. New research on how to manipulate the microbiome for better detection and treatment of endometriosis is emerging.
Introduction
The evidence on eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) intake status and long-term mortality among people with diabetes is scarce. This study aimed to investigate the relationship between EPA and DHA intakes with all-cause and cause-specific mortality in adults with diabetes.
Methods
This study included 2,991 adults with diabetes from the National Health and Nutrition Examination Survey (NHANES) 1999–2008. Death outcomes were ascertained by linkage to the database records through 31 December 2015. Cox proportional hazards regression models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for mortality from all causes, cardiovascular disease (CVD), and coronary heart disease (CHD) in patients with diabetes.
Results
Among 2,991 patients with diabetes, the mean age was 61.9 years (55.2% males). During the mean follow-up duration of 9.4 years, a total of 1,091 deaths were documented, of which 273 were due to CVD, including 227 CHD deaths. EPA and DHA intakes were associated with lower mortality risks, especially that of CVD. After adjusting for demographic, major lifestyle factors, overall dietary intake patterns, and history of hypertension and dyslipidemia, the multivariable HRs (95% CIs) of mortality risk comparing Q4 to Q1 of EPA intake were 0.55 (0.33–0.92; P -trend = 0.019) for CHD, 0.55 (0.36–0.83; P -trend = 0.005) for CVD, and 0.91 (0.70–1.18; P -trend = 0.264) for all-cause. The respective HRs (95% CIs) comparing Q4 to Q1 of DHA were 0.60 (0.37–0.98; P -trend = 0.051) for CHD, 0.58 (0.38–0.89; P -trend = 0.014) for CVD, and 0.92 (0.72–1.18; P -trend = 0.481) for all-cause. In subgroup analysis, we found that the association trends of EPA and DHA intakes with death risk remained robust among patients with diabetes, especially among those who are old, female, those with higher BMI, and dyslipidemia patients with CVD and CHD.
Discussion
In the USA, higher EPA and DHA intakes were associated with a lower risk of CHD and CVD mortality in patients with diabetes. Our study supports the benefits of adequate EPA and DHA intakes in promoting the health of patients with diabetes.
The purpose of this study was to determine anti-inflammatory and/or chondroprotective effects of Equine Omega Complete (EOC) on cartilage explants stimulated with lipopolysaccharide (LPS). Explants were aseptically prepared from the intercarpal joints of 17 market-weight pigs and placed in culture at 37°C for a total of 120 hours. For the final 96 hours, explants were conditioned with a simulated digestion extract of EOC (0, 36 or 180 μL/mL), and for the final 48 hours explants were stimulated with LPS (0 or 15µg/mL). Media was removed and replaced every 24 hours. Samples from the final 48 hours were analyzed for biomarkers of cartilage inflammation [prostaglandin E2 (PGE2) and nitric oxide (NO)] and cartilage structure [glycosaminoglycan (GAG)]. At the end of the culture period cartilage explants were stained for an estimate of cell viability. Stimulation of unconditioned explants with LPS significantly increased media concentrations of PGE2, GAG and NO compared with that from unstimulated explants. LPS stimulation did not significantly affect cell viability. Both concentrations of EOC prevented significant LPS-stimulated cartilage release of GAG without impairing chondrocyte viability. No other effects of treatment were observed. These data provide evidence for a non-cytotoxic, chondroprotective effect of EOC in cartilage. This in vitro experiment supports the use of EOC in protecting against the detrimental effects of inflammation on cartilage structure.
Schizophrenia (SZ) is a serious neurodevelopmental disorder. As the etiology of SZ is complex and the pathogenesis is not thoroughly understood, the diagnosis of different subtypes still depends on the subjective judgment of doctors. Therefore, there is an urgent need to develop early objective laboratory diagnostic biomarkers to screen different subtypes of patients as early as possible, and to implement targeted prevention and precision medicine to reduce the risk of SZ and improve patients’ quality of life. In this study, untargeted metabolomics and 16S rDNA sequencing were used to analyze the differences in metabolites and gut microflora among 28 patients with two types of schizophrenia and 11 healthy subjects. The results showed that the metabolome and sequencing data could effectively discriminate among paranoid schizophrenia patients, undifferentiated schizophrenia patients and healthy controls. We obtained 65 metabolites and 76 microorganisms with significant changes, and fecal metabolite composition was significantly correlated with the differential genera (|r|>0.5), indicating that there was a regulatory relationship between the gut microbiota and the host metabolites. The gut microbiome, as an objective and measurable index, showed good diagnostic value for distinguishing schizophrenia patients from healthy people, especially with a combination of several differential microorganisms, which had the best diagnostic effect (AUC>0.9). Our results are conducive to understanding the complicated metabolic changes in SZ patients and providing valuable information for the clinical diagnosis of SZ.
Omega-3 polyunsaturated fatty acids (omega-3 PUFAs) are essential for improving the health and performance of athletes. The present study aimed to evaluate the nutritional status of omega-3 PUFAs in Chinese elite athletes by both dietary intake analysis and serum biomarker detection. A cross-sectional analysis of data from 54 elite athletes (24 men and 30 women) from Shanghai professional sports teams was conducted. A food frequency questionnaire (FFQ) was employed to analyze dietary intake, and gas chromatography-mass spectrometry (GC-MS/MS) was conducted to measure serum biomarkers of PUFAs. Correlation analysis was performed to investigate the relationships of PUFA biomarkers with diet, inflammation and oxidative stress. The results showed that the median intake of EPA + DHA among athletes was 132 mg/d, which is lower than the minimum value recommended by dietary guidelines (250 mg/d). The average serum EPA + DHA was 4.0 ± 1.1%, and the ratio of omega-6/omega-3 was 7.7 ± 1.7. Most (96.3%) of the athletes were below the targeted value of serum EPA + DHA, which is associated with a reduction in cardiovascular risk. Correlation analysis showed that the serum EPA + DHA was positively correlated with the long-term dietary intake of EPA + DHA and negatively correlated with inflammatory markers. In conclusion, the serum circulating EPA + DHA and omega-6/omega-3 ratio are effective biomarkers reflecting the nutritional status of PUFAs in athletes. Omega-3 PUFAs have a potential effect on inhibiting inflammatory markers. Hence, it is necessary for Chinese athletes to improve their suboptimal nutritional status of PUFAs through dietary intervention.
Modification of vegetable oils is carried out to make them suitable according to their specific end use as most of the vegetable oils in original forms do not meet the recommended dietary allowance of saturated (SFA), monounsaturated (MUFA) and polyunsaturated (PUFA) fatty acids. Vegetable oils are modified using a variety of techniques including hydrogenation, interesterification, fractionation, and blending. However, blending is the most widely accepted method for improving the physicochemical properties, nutritive value and oxidative stability of vegetable oils because it is simple, cost-effective, non-destructive, and does not involve chemical treatments. Blending vegetable oils with contrasting fatty acid compositions or blending omega 3 fatty acids and antioxidants rich minor oils with major oils are two common strategies to formulate blends. Blended oil with balanced fatty acids could play substantial role in improving the consumers’ health. However, while designing vegetable oil blends, it is important to keep in mind the intended application of the formulated blend, consumer’s demands and also food laws. This review paper covers the literature related to blending of vegetable oils with a focus on effect of vegetable oils blending on their physicochemical and nutritional properties, health benefits and utility in food industries.
In this study, novel Poria cocos oligosaccharides (PCO) were prepared by enzymatic degradation, and their polymerization degree was determined to be 2-6 by LC-MS analysis. By monosaccharide composition analysis, methylation assay, FT-IR, and NMR analysis, PCO were deduced to contain the sugar residues of (1 → 2)-β-D-Glcp, (1 → 2)-α-D-Glcp, and (1 → 4)-α-D-Glcp. Using an HFD-fed mouse model with dyslipidemia, PCO could significantly suppress lipid metabolism disorders, characterized by the reduction of lipid accumulation and inflammatory responses in the blood and liver tissues. Based on the non-targeted metabolomic analysis and Spearman's correlation analysis, we presume that the preventive effect of PCO on dyslipidemia might contribute to the reversal of changed metabolic pathways, which were related to the metabolisms of glycerophospholipids, unsaturated fatty acids, amino acids, choline, bile acids, tryptophan, sphingolipids, and glutathione. Our research shed light on the potential application of PCO for the treatment of dyslipidemia.
Low-carbohydrate and high-fat diets have been used for body weight (BW) control, but their adverse effects on lipid profiles have raised concern. Fish oil (FO), rich in omega-3 polyunsaturated fatty acids, has profound effects on lipid metabolism. We hypothesized that FO supplementation might improve the lipid metabolic disturbance elicited by low-carbohydrate and high-fat diets. Male SD rats were randomized into normal control diet (NC), high-fat diet (HF), and low-carbohydrate/high-fat diet (LC) groups in experiment 1, and NC, LC, LC + 5% FO (5CF), and LC + 10% FO diet (10CF) groups in experiment 2. The experimental duration was 11 weeks. In the LC group, a ketotic state was induced, and food intake was decreased; however, it did not result in BW loss compared to either the HF or NC groups. In the 5CF group, rats lost significant BW. Dyslipidemia, perirenal and epididymal fat accumulation, hepatic steatosis, and increases in triglyceride and plasma leptin levels were observed in the LC group but were attenuated by FO supplementation. These findings suggest that a ketogenic low-carbohydrate/high-fat diet with no favorable effect on body weight causes visceral and liver lipid accumulation. FO supplementation not only aids in body weight control but also improves lipid metabolism in low-carbohydrate/high-fat diet-fed rats.
Keluoxin (KLX) is an active agent in the treatment of diabetic retinopathy (DR). However, its mechanism, targets, and effective constituents against DR are still unclear, which seriously restricts its clinical application. Chinmedomics has the promise of explaining the pharmacological effects of herbal medicines and investigating the effective mechanisms. The research results from electroretinography and electron microscope showed that KLX could reduce retinal dysfunction and pathological changes by the DR mouse model. Based on effectiveness, we discovered 64 blood biomarkers of DR by nontargeted metabolomics analysis, 51 of which returned to average levels after KLX treatment including leukotriene D4 and A4, l -tryptophan, 6-hydroxymelatonin, l -phenylalanine, l -tyrosine, and gamma-linolenic acid (GLA). The metabolic pathways involved were phenylalanine metabolism, steroid hormone biosynthesis, sphingolipid metabolism, etc. Adenosine monophosphate-activated protein kinase (AMPK), extracellular signal-regulated protein kinase1/2 (ERK1/2), phosphatidylinositol-3-kinase (PI3K), and protein 70 S6 kinase (p70 S6K) might be potential targets of KLX against DR. This was related to the mammalian target of rapamycin (mTOR) signaling and AMPK signaling pathways. We applied the chinmedomics strategy, integrating serum pharm-chemistry of traditional Chinese medicine (TCM) with metabolomics, to discover astragaloside IV (AS-IV), emodin, rhein, chrysophanol, and other compounds, which were the core effective constituents of KLX when against DR. Our study was the first to apply the chinmedomics strategy to discover the effective constituents of KLX in the treatment of DR, which fills the gap of unclear effective constituents of KLX. In the next step, the research of effective constituents can be used to optimize prescription preparation, improve the quality standard, and develop an innovative drug.
Ischemic heart disease is very uncommon in Greenland Eskimos (Harvald, 1974). In his extensive nosography of Greenland, Berthelsen (1940) does not even mention this disease, although he gives some information on atherosclerosis in Greenlanders. Other thrombotic diseases, in both the arterial and the venous systems, are mentioned either very infrequently by him or not at all. In the annual report on the state of health in Greenland (Bøggild et al., 1978) covering the years 1973–1976, death from ischemic heart diseases constitutes an average of 3.5% of all causes of death. In this and in other official medical statistics, no distinction is made between true Greenlanders and Danish workers who spend various amounts of time in Greenland, but who almost invariably carry their Western way of life with them. However, this fraction of the total population of nearly 50,000 inhabitants on this huge island of 2,175,000 km2 is small. Life expectancy rapidly increased in the more than 60 years since tuberculosis was successfully defeated. The most common cause of death is still accidents, amounting to about one-third of all deaths. The same statistical source reports an annual average of 9 1/2 cases of myocardial infarction among hospitalized patients in Greenland. The majority of these, as well as of the deaths reportedly caused by ischemic heart diseases, is from the southern and most “Westernized” part of Greenland, whereas from 1968 to 1978, not a single death from ischemic heart disease or case of myocardial infarction was reported from the UmanaK district (population of about 2600) where the present investigations were carried out.
Background/Objectives
There is growing evidence that early development of obesity increases cardiovascular risk later in life, but less is known about whether there are effects of long-term excess body weight on the biological drivers associated with the atherosclerotic pathway, particularly adipokines, inflammatory and endothelial markers. This paper therefore investigates the influence of overweight across the life course on levels of these markers at retirement age.Subjects/Methods
Data from the MRC National Survey of Health and Development (n=1784) were used to examine associations between overweight status at 2, 4, 6, 7, 11, 15, 20, 26, 36, 43, 53 and 60-64 years (BMI⩾25 kg/m(2) for adult ages and gender-specific cut-points for childhood ages equivalent to BMI⩾25 kg/m(2)) and measurements of adipokines (leptin, adiponectin), inflammatory markers (C-reactive protein [CRP], Interleukin-6 [IL-6]) and endothelial markers (E-selectin, tissue plasminogen activator [t-PA] and von Willebrand factor) at 60-64 years. Additionally, the fit of different life course models (sensitive periods/accumulation) was compared using partial F-tests.ResultsIn age and sex-adjusted models, overweight at 11 years and onwards was associated with higher leptin, CRP and IL-6 and lower adiponectin; overweight at 15 years and onwards with higher E-selectin and t-PA. Associations between overweight at all ages earlier than 60-64 with leptin, adiponectin, CRP and IL-6 were reduced but remained apparent after adjustment for overweight at 60-64 years; while those with E-selectin and t-PA were entirely explained. An accumulation model best described the associations between overweight across the life course with adipokines and inflammatory markers, while for the endothelial markers the sensitive period model for 60-64 years provided a slightly better fit than the accumulation model.Conclusions
Overweight across the life course has a cumulative influence on adipokines, inflammatory and possibly endothelial markers. Avoidance of overweight from adolescence onwards is likely important for cardiovascular disease prevention.International Journal of Obesity accepted article preview online, 13 February 2015. doi:10.1038/ijo.2015.19.
Nutritional factors such as casein hydrolysates and long chain polyunsaturated fatty acids have been proposed to exert beneficial metabolic effects. We aimed to investigate how a casein hydrolysate (eCH) and long chain polyunsaturated fatty acids could affect human primary adipocyte function in vitro. Incubation conditions with the different nutritional factors were validated by assessing cell vitality with lactate dehydrogenase (LDH) release and neutral red incorporation. Intracellular triglyceride content was assessed with Oil Red O staining. The effect of eCH, a non-peptidic amino acid mixture (AA), and long-chain polyunsaturated fatty acids (LC-PUFAs) on adiponectin and leptin secretion was determined by enzyme-linked immunosorbent assay (ELISA). Intracellular adiponectin expression and nuclear factor-κB (NF-κB) activation were analyzed by Western blot, while monocyte chemoattractant protein-1 (MCP-1) release was explored by ELISA. The eCH concentration dependently increased adiponectin secretion in human primary adipocytes through its intrinsic peptide bioactivity, since the non-peptidic mixture, AA, could not mimic eCH's effects on adiponectin secretion. Eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and DHA combined with arachidonic acid (ARA) upregulated adiponectin secretion. However, only DHA and DHA/ARA exerted a potentanti-inflammatory effect reflected by prevention of tumor necrosis factor-α (TNF-α) induced NF-κB activation and MCP-1 secretion in human adipocytes. eCH and DHA alone or in combination with ARA, may hold the key for nutritional programming through their anti-inflammatory action to prevent diseases with low-grade chronic inflammation such as obesity or diabetes.
Abstract
CONTEXT:
Postoperative atrial fibrillation or flutter (AF) is one of the most common complications of cardiac surgery and significantly increases morbidity and health care utilization. A few small trials have evaluated whether long-chain n-3-polyunsaturated fatty acids (PUFAs) reduce postoperative AF, with mixed results.
OBJECTIVE:
To determine whether perioperative n-3-PUFA supplementation reduces postoperative AF.
DESIGN, SETTING, AND PATIENTS:
The Omega-3 Fatty Acids for Prevention of Post-operative Atrial Fibrillation (OPERA) double-blind, placebo-controlled, randomized clinical trial. A total of 1516 patients scheduled for cardiac surgery in 28 centers in the United States, Italy, and Argentina were enrolled between August 2010 and June 2012. Inclusion criteria were broad; the main exclusions were regular use of fish oil or absence of sinus rhythm at enrollment.
INTERVENTION:
Patients were randomized to receive fish oil (1-g capsules containing ≥840 mg n-3-PUFAs as ethyl esters) or placebo, with preoperative loading of 10 g over 3 to 5 days (or 8 g over 2 days) followed postoperatively by 2 g/d until hospital discharge or postoperative day 10, whichever came first.
MAIN OUTCOME MEASURE:
Occurrence of postoperative AF lasting longer than 30 seconds. Secondary end points were postoperative AF lasting longer than 1 hour, resulting in symptoms, or treated with cardioversion; postoperative AF excluding atrial flutter; time to first postoperative AF; number of AF episodes per patient; hospital utilization; and major adverse cardiovascular events, 30-day mortality, bleeding, and other adverse events.
RESULTS:
At enrollment, mean age was 64 (SD, 13) years; 72.2% of patients were men, and 51.8% had planned valvular surgery. The primary end point occurred in 233 (30.7%) patients assigned to placebo and 227 (30.0%) assigned to n-3-PUFAs (odds ratio, 0.96 [95% CI, 0.77-1.20]; P = .74). None of the secondary end points were significantly different between the placebo and fish oil groups, including postoperative AF that was sustained, symptomatic, or treated (231 [30.5%] vs 224 [29.6%], P = .70) or number of postoperative AF episodes per patient (1 episode: 156 [20.6%] vs 157 [20.7%]; 2 episodes: 59 [7.8%] vs 49 [6.5%]; ≥3 episodes: 18 [2.4%] vs 21 [2.8%]) (P = .73). Supplementation with n-3-PUFAs was generally well tolerated, with no evidence for increased risk of bleeding or serious adverse events.
CONCLUSION:
In this large multinational trial among patients undergoing cardiac surgery, perioperative supplementation with n-3-PUFAs, compared with placebo, did not reduce the risk of postoperative AF. TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00970489.
Comment in
Fish oil vs olive oil for postoperative atrial fibrillation. [JAMA. 2013]
Fish oil vs olive oil for postoperative atrial fibrillation--reply. [JAMA. 2013]
PMID: 23128104 [PubMed - indexed for MEDLINE] PMCID: PMC3694745 Free PMC Article
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Sepsis rapidly activates the host inflammatory response and acute phase response. Severe sepsis, complicated by multiple organ failure, is associated with overwhelming inflammation and high mortality. We previously observed that zinc (Zn) deficiency significantly increases mortality in a mouse model of polymicrobial sepsis due to over-activation of the inflammatory response. In order to identify potential mechanisms that account for Zn-responsive effects, we generated whole exome expression profiles from the lung tissue of septic mice that were maintained on Zn modified diets. Based on systems analysis, we observed that Zn deficiency enhances the acute phase response and particularly the JAK-STAT3 pathway, resulting in increased serum amyloid A production. In vitro studies of primary hepatocytes and HepG2 cells substantiated that Zn-deficiency augments serum amyloid A production through up-regulation of the JAK-STAT3 and NF-κB pathways. In contrast, Zn inhibited STAT3 activation through the up-regulation of SHP1 activity. Collectively, these findings demonstrate that Zn deficiency enhances the acute phase response through up-regulation of the JAK-STAT3 pathway, thereby perpetuating increased inflammation that may lead to increased morbidity and mortality in response to sepsis.
The objective of the present study was to investigate the optimal dietary n-6:n-3 PUFA ratios that regulate lipid metabolism and inflammation in pigs. A total of ninety-six cross-bred (Large White × Landrace) growing-finishing pigs (73·8 (sem 1·6) kg) were chosen and fed one of the four isoenergetic diets with n-6:n-3 PUFA ratios of 1:1, 2·5:1, 5:1 and 10:1. The growth performance of pigs fed the diet with an n-6:n-3 PUFA ratio of 5:1 was the best, but the group fed the diet with an n-6:n-3 PUFA ratio of 1:1 had the highest muscle mass and the lowest adipose tissue mass (P< 0·05). The concentrations of IL-6 and IL-1β of pigs fed the diet with an n-6:n-3 PUFA ratio of 1:1 were decreased compared with those of the other groups (P< 0·05). The concentration of adiponectin of pigs fed the diet with an n-6:n-3 PUFA ratio of 1:1 was also markedly decreased, but the concentration of leptin was increased compared with that of the groups fed the diets with n-6:n-3 PUFA ratios of 5:1 and 10:1 (P< 0·05). Additionally, the optimal dietary ratios of n-6:n-3 PUFA of 1:1 and 5:1 markedly suppressed the expression levels of lipid metabolism-related genes and proteins such as phosphoinositide-3-kinase-α, fatty acid transport protein-1 and PPARγ. They also significantly suppressed the expression levels of the inflammatory cytokines IL-1β, TNF-α and IL-6. The results indicated that the optimal n-6:n-3 PUFA ratios of 1:1 and 5:1 exerted beneficial effects on lipid metabolism and inflammatory system, leading to the availability of more energy and nutrients for high performance and homeostatic pathways.
BACKGROUND: Observational cohort studies and a secondary prevention trial have shown an inverse association between adherence to the Mediterranean diet and cardiovascular risk. We conducted a randomized trial of this diet pattern for the primary prevention of cardiovascular events.
METHODS: In a multicenter trial in Spain, we randomly assigned participants who were at high cardiovascular risk, but with no cardiovascular disease at enrollment, to one of three diets: a Mediterranean diet supplemented with extra-virgin olive oil, a Mediterranean diet supplemented with mixed nuts, or a control diet (advice to reduce dietary fat). Participants received quarterly individual and group educational sessions and, depending on group assignment, free provision of extra-virgin olive oil, mixed nuts, or small nonfood gifts. The primary end point was the rate of major cardiovascular events (myocardial infarction, stroke, or death from cardiovascular causes). On the basis of the results of an interim analysis, the trial was stopped after a median follow-up of 4.8 years.
RESULTS: A total of 7447 persons were enrolled (age range, 55 to 80 years); 57% were women. The two Mediterranean-diet groups had good adherence to the intervention, according to self-reported intake and biomarker analyses. A primary end-point event occurred in 288 participants. The multivariable-adjusted hazard ratios were 0.70 (95% confidence interval [CI], 0.54 to 0.92) and 0.72 (95% CI, 0.54 to 0.96) for the group assigned to a Mediterranean diet with extra-virgin olive oil (96 events) and the group assigned to a Mediterranean diet with nuts (83 events), respectively, versus the control group (109 events). No diet-related adverse effects were reported.
CONCLUSIONS: Among persons at high cardiovascular risk, a Mediterranean diet supplemented with extra-virgin olive oil or nuts reduced the incidence of major cardiovascular events. (Funded by the Spanish government's Instituto de Salud Carlos III and others; Controlled-Trials.com number, ISRCTN35739639.).
Background
Growing evidence suggests a cardioprotective role of omega-3 polyunsaturated fatty acids (PUFA). However, the exact mechanisms underlying the effects of omega-3 PUFA in humans have not yet been fully clarified.
Purpose
We sought to evaluate omega-3 PUFA-mediated effects on adipokines in patients with stable coronary artery disease (CAD) undergoing elective percutaneous coronary intervention (PCI).
Methods
We conducted a prospective, double-blind, placebo-controlled, randomized study, in which adiponectin, leptin and resistin were determined at baseline, 3–5 days and 30 days during administration of omega-3 PUFA 1 g/day (n = 20) or placebo (n = 28).
Results
As compared to controls administration of omega-3 PUFA resulted in increase of adiponectin by 13.4 % (P < 0.0001), reduction of leptin by 22 % (P < 0.0001) and increase of adiponectin to leptin (A/L) ratio by 45.5 % (P < 0.0001) at 30 days, but not at 3–5 days. Compared with placebo adiponectin was 12.7 % higher (P = 0.0042), leptin was 16.7 % lower (P < 0.0001) and A/L ratio was 33.3 % higher (P < 0.0001) in the omega-3 PUFA group at 30 days. Resistin decreased similarly in both groups after 1 month, without intergroup differences (P = 0.32). The multivariate model showed that the independent predictors of changes in adiponectin at 1 month (P < 0.001) were: omega-3 PUFA treatment, baseline platelet count, total cholesterol and those in leptin (P < 0.0001) were: omega-3 PUFA treatment and waist circumference. Independent predictors of A/L ratio changes (P < 0.0001) were: assigned treatment, current smoking and hyperlipidemia.
Conclusions
In high risk stable coronary patients after PCI omega-3 PUFA supplementation improves adipokine profile in circulating blood. This might be a novel, favourable mechanism of omega-3 PUFA action.
Context Postoperative atrial fibrillation or flutter (AF) is one of the most common complications of cardiac surgery and significantly increases morbidity and health care utilization. A few small trials have evaluated whether long-chain n-3-polyunsaturated fatty acids (PUFAs) reduce postoperative AF, with mixed results.
Objective To determine whether perioperative n-3-PUFA supplementation reduces postoperative AF.
Design, Setting, and Patients The Omega-3 Fatty Acids for Prevention of Post-operative Atrial Fibrillation (OPERA) double-blind, placebo-controlled, randomized clinical trial. A total of 1516 patients scheduled for cardiac surgery in 28 centers in the United States, Italy, and Argentina were enrolled between August 2010 and June 2012. Inclusion criteria were broad; the main exclusions were regular use of fish oil or absence of sinus rhythm at enrollment.
Intervention Patients were randomized to receive fish oil (1-g capsules containing ≥840 mg n-3-PUFAs as ethyl esters) or placebo, with preoperative loading of 10 g over 3 to 5 days (or 8 g over 2 days) followed postoperatively by 2 g/d until hospital discharge or postoperative day 10, whichever came first.
Main Outcome Measure Occurrence of postoperative AF lasting longer than 30 seconds. Secondary end points were postoperative AF lasting longer than 1 hour, resulting in symptoms, or treated with cardioversion; postoperative AF excluding atrial flutter; time to first postoperative AF; number of AF episodes per patient; hospital utilization; and major adverse cardiovascular events, 30-day mortality, bleeding, and other adverse events.
Results At enrollment, mean age was 64 (SD, 13) years; 72.2% of patients were men, and 51.8% had planned valvular surgery. The primary end point occurred in 233 (30.7%) patients assigned to placebo and 227 (30.0%) assigned to n-3-PUFAs (odds ratio, 0.96 [95% CI, 0.77-1.20]; P = .74). None of the secondary end points were significantly different between the placebo and fish oil groups, including postoperative AF that was sustained, symptomatic, or treated (231 [30.5%] vs 224 [29.6%], P = .70) or number of postoperative AF episodes per patient (1 episode: 156 [20.6%] vs 157 [20.7%]; 2 episodes: 59 [7.8%] vs 49 [6.5%]; ≥3 episodes: 18 [2.4%] vs 21 [2.8%]) (P = .73). Supplementation with n-3-PUFAs was generally well tolerated, with no evidence for increased risk of bleeding or serious adverse events.
Conclusion In this large multinational trial among patients undergoing cardiac surgery, perioperative supplementation with n-3-PUFAs, compared with placebo, did not reduce the risk of postoperative AF.
Trial Registration clinicaltrials.gov Identifier: NCT00970489
In obesity, the adipose cells behave as inflammatory source and result to low grade inflammation. This systemic inflammation along with oxidative stress is a silent killer and damages other vital organs also. High metabolic process, induced due to high nutritional intake, results to endoplasmic reticulum (ER) stress and mitochondrial stress. This review describes the triggering factor and basic mechanism behind the obesity mediated these stresses in relation to inflammation. Efforts have been made to describe the effect-response cycle between adipocytes and non-adipocyte cells with reference to metabolic syndrome (MS).
Atrial fibrillation (AF) is an increasingly common arrhythmia that now stands at epidemic proportion, with more than 2.3 million
people affected in the USA and over 4.5 million people affected in Western Europe. AF is an expression of underlying heart
disease and is increasingly associated with hypertension, congestive heart failure, and ischemic heart disease. It is also
a progressive disease secondary to continuous structural remodeling of the atria, which relates to AF itself, to changes associated
with aging and to progression of the underlying heart disease. Traditionally, AF has been addressed only after it has already
presented with pharmacological and nonpharmacological therapies designed for rhythm or rate control (secondary prevention).
Although secondary prevention is the most feasible approach at present, the concept of primary prevention of AF with therapies
aimed at preventing the development of substrate and correcting the risk factors for AF has emerged as a strategy, which is
likely to produce a larger effect in the general population. Recent experiments provided new insights into AF pathophysiology,
which generated background for new mechanism-based therapies. Agents targeting inflammation, oxidative injury, atrial myocyte
metabolism, extracellular matrix remodeling, and fibrosis have theoretical advantages as novel therapeutic strategies. In
this respect, drugs that are not traditionally antiarrhythmic such as angiotensin-converting enzyme inhibitors, angiotensin-receptor
blockers, aldosterone antagonists, statins, and omega-3 polyunsaturated fatty acids have shown an antiarrhythmic potential
in addition to any treatment effect on the underlying disease. These agents are thought to have an advantage of targeting
both the occurrence and progression of the substrate for AF, thus, providing primary and secondary prevention of the arrhythmia.
Although first experimental and hypothesis-generating small clinical studies or retrospective analyses have been encouraging,
several larger, properly designed, prospective trials have not confirmed earlier observations. This review provides a contemporary
evidence-based insight into the possible preventative and reverse remodeling role of statins and polyunsaturated fatty acids
in AF.
N-3 Polyunsaturated fatty acids (n-3 PUFA) exert clinical beneficial effects in patients after acute myocardial infarction (AMI). However, their exact mechanisms of action are not well recognized yet. Our aim was to evaluate effects of early introduced n-3 PUFA supplementation on endothelial function and serum adipokine concentrations in patients with AMI.
Thirty-eight patients with AMI and successful coronary stent implantation were randomized to the study group (PUFA group: n = 19; standard therapy + PUFA 1 g daily) and the control group (control group: n = 19; standard therapy). The study group patients were given n-3 PUFA (Omacor 1 g daily) starting from the 3(rd) day of AMI. Ultrasound vascular indexes (flow-mediated dilatation [FMD], nitroglycerine-mediated dilation [NMD]) and serum concentrations of adiponectin and resistin (ELISA) were evaluated before and after 30 days of pharmacotherapy.
Comparison of the mean delta values (baseline/after 30 days of therapy) between groups revealed significant differences for delta FMD (PUFA 7.6 ±12.4% vs. control -1.7 ±10.5%, p = 0.019) and delta resistin concentrations (PUFA 1.0 ±3.8pg/ml vs. control -1.6 ±2.9pg/ml, p = 0.028). Multiple linear regression analysis for all subjects revealed the n-3 PUFA supplementation (r = 10.933, p = 0.004) and waist circumference (r = -0.467, p = 0.01) as independent factors associated with delta FMD values (R-adjusted 0.29; p = 0.002).
Early and short-term n-3 PUFA supplementation in AMI with successful primary PCI and optimal pharmacotherapy improves endothelial function. However, increased resistin serum levels observed after 1-month n-3 PUFA supplementation merits further investigations.
Obesity leads to several chronic morbidities including type 2 diabetes, dyslipidaemia, atherosclerosis and hypertension, which are major components of the metabolic syndrome. White adipose tissue (WAT) metabolism and WAT-derived factors (fatty acids and adipokines) play an important role in the development of these metabolic disturbances. In fact, dysregulated adipokine secretion from the expanded WAT of obese individuals contributes to the development of systemic low-grade inflammation, insulin resistance and metabolic syndrome. The n-3 PUFA EPA and DHA have been widely reported to have protective effects in a range of chronic inflammatory conditions including obesity. In fact, n-3 PUFA have been shown to ameliorate low-grade inflammation in adipose tissue associated with obesity and up-regulate mitochondrial biogenesis and induce beta-oxidation in WAT in mice. Moreover, the ability of n-3 PUFA to regulate adipokine gene expression and secretion has been observed both in vitro and in vivo in rodents and human subjects. The present article reviews: (1) the physiological role of adiponectin, leptin and pre-B cell colony-enhancer factor/visfatin, three adipokines with immune-modulatory properties involved in the regulation of metabolism and insulin sensitivity and (2) the actions of n-3 PUFA on these adipokines focusing on the underlying mechanisms and the potential relationship with the beneficial effects of these fatty acids on obesity-associated metabolic disorders. It can be concluded that the ability of n-3 PUFA to improve obesity and insulin resistance conditions partially results from the modulation of WAT metabolism and the secretion of bioactive adipokines including leptin, adiponectin and visfatin.
Adiponectin has insulin-sensitizing, anti-atherogenic, and anti-inflammatory properties, and researchers have recently reported that omega-3 polyunsaturated fatty acid (PUFA) can increase the serum adiponectin concentration, suggesting that dietary factors, such as fish intake, may have an influence on the serum adiponectin concentration. In general, Japanese subjects consume twice as much fish as people in other countries. We hypothesized that incremental change in serum omega-3 PUFA levels by fish intake is an important regulator of serum adiponectin even in Japanese subjects. The aim of this study was to explore the relationship among fish consumption, serum omega-3 PUFA, such as eicosapentaenoic acid (EPA), levels, and serum adiponectin levels.
We recruited 17 healthy Japanese volunteers (seven men and 10 women) for an 8-week fish-diet intervention (omega-3 PUFA 3.0 g/day) without affecting total energy intake, and measured serum adiponectin concentration and fatty acid profiles.
Fish-diet intervention significantly increased the serum adiponectin concentration in women (from 13.5+/-4.6 to 15.8+/-5.2 microg/mL, p <0.01) but not in men (from 8.7+/-2.8 to 8.7+/-2.5 microg/mL). Serum omega-3 PUFA increased more in female subjects than male subjects after the fish-diet intervention (57.3+/-86.6 vs 150.9+/-46.7 microg/mL, p=0.011), suggesting that changes in omega-3 PUFA concentration may explain the different response between sexes.
A fish-based diet intervention increased the serum adiponectin concentration in young, non-obese, healthy Japanese female subjects. The increment in serum omega-3 PUFA may regulate the serum adiponectin concentration.
Higher consumption of fish and omega-3 fatty acids has been associated with a lower risk of coronary heart disease (CHD) in men, but limited data are available regarding women.
To examine the association between fish and long-chain omega-3 fatty acid consumption and risk of CHD in women.
Dietary consumption and follow-up data from 84 688 female nurses enrolled in the Nurses' Health Study, aged 34 to 59 years and free from cardiovascular disease and cancer at baseline in 1980, were compared from validated questionnaires completed in 1980, 1984, 1986, 1990, and 1994.
Incident nonfatal myocardial infarction and CHD deaths.
During 16 years of follow-up, there were 1513 incident cases of CHD (484 CHD deaths and 1029 nonfatal myocardial infarctions). Compared with women who rarely ate fish (<1 per month), those with a higher intake of fish had a lower risk of CHD. After adjustment for age, smoking, and other cardiovascular risk factors, the multivariable relative risks (RRs) of CHD were 0.79 (95% confidence interval [CI], 0.64-0.97) for fish consumption 1 to 3 times per month, 0.71 (95% CI, 0.58-0.87) for once per week, 0.69 (95% CI, 0.55-0.88) for 2 to 4 times per week, and 0.66 (95% CI, 0.50-0.89) for 5 or more times per week (P for trend =.001). Similarly, women with a higher intake of omega-3 fatty acids had a lower risk of CHD, with multivariable RRs of 1.0, 0.93, 0.78, 0.68, and 0.67 (P<.001 for trend) across quintiles of intake. For fish intake and omega-3 fatty acids, the inverse association appeared to be stronger for CHD deaths (multivariate RR for fish consumption 5 times per week, 0.55 [95% CI, 0.33-0.90] for CHD deaths vs 0.73 [0.51-1.04]) than for nonfatal myocardial infarction.
Among women, higher consumption of fish and omega-3 fatty acids is associated with a lower risk of CHD, particularly CHD deaths.
The immune system, including its inflammatory components, is fundamental to host defence against pathogenic invaders. It is a complex system involving interactions amongst many different cell types dispersed throughout the body. Central to its actions are phagocytosis of bacteria, processing of antigens derived from intracellular and extracellular pathogens, activation of T cells with clonal expansion (proliferation) and production of cytokines that elicit effector cell functions such as antibody production and killing cell activity. Inappropriate immunologic activity, including inflammation, is a characteristic of many common human disorders. Eicosanoids produced from arachidonic acid have roles in inflammation and regulation of T and B lymphocyte functions. Eicosapentaenoic acid (EPA) also gives rise to eicosanoids and these may have differing properties from those of arachidonic acid-derived eicosanoids. EPA and docosahexaenoic acid (DHA) give rise to newly discovered resolvins which are anti-inflammatory and inflammation resolving. Human immune cells are typically rich in arachidonic acid, but arachidonic acid, EPA and DHA contents can be altered through oral administration of EPA and DHA. This results in a changed pattern of production of eicosanoids and probably also of resolvins, although the latter are not well examined in the human context. Changing the fatty acid composition of immune cells also affects phagocytosis, T cell signaling and antigen presentation capability. These effects appear to mediated at the membrane level suggesting important roles of fatty acids in membrane order, lipid raft structure and function, and membrane trafficking. Thus, the fatty acid composition of human immune cells influences their function and the cell membrane contents of arachidonic acid, EPA and DHA are important. Fatty acids influence immune cell function through a variety of complex mechanisms and these mechanisms are now beginning to be unraveled
Background There is conflicting evidence on the benefits of foods rich in vitamin E (alpha-tocopherol), n-3 polyunsaturated fatty acids (PUFA), and their pharmacological substitutes. We investigated the effects of these substances as supplements in patients who had myocardial infarction. Methods From October, 1993, to September, 1995, 11324 patients surviving recent (less than or equal to 3 months) myocardial infarction were randomly assigned supplements of n-3 PUFA (Ig daily, n=2836), vitamin E (300 mg daily, n=2830), both (n=2830), or none (control, n=2828) for 3.5 years. The primary combined efficacy endpoint was death, non-fatal myocardial infarction, and stroke. Intention-to-treat analyses were done according to a factorial design (two-way) and by treatment group (four-way). Findings Treatment with n-3 PUFA, but not vitamin E, significantly lowered the risk of the primary endpoint (relative risk decrease 10% [95% CI 1-18] by two-way analysis, 15% [2-26] by four-way analysis). Benefit was attributable to a decrease in the risk of death (14% [3-24] two-way, 20% [6-33] four-way) and cardiovascular death (17% [3-29] two-way, 30% [13-44] four-way). The effect of the combined treatment was similar to that for n-3 PUFA for the primary endpoint (14% [1-26]) and for fatal events (20% [5-33]). Interpretation Dietary supplementation with n-3 PUFA led to a clinically important and satistically significant benefit. Vitamin E had no benefit. Its effects on fatal cardiovascular events require further exploration.
Background: Previous randomized studies have reported conlicting results on the eficacy of omega-3 fatty acids (PUFA) in preventing atrial ibrillation (AF) post cardiac surgery. Therefore, a meta-analysis of the role of PUFA in the prevention of atrial ibrillation in post-cardiac surgery patients was conducted.
The National Cholesterol Education Program’s Adult Treatment Panel III report (ATP III)1 identified the metabolic syndrome as a multiplex risk factor for cardiovascular disease (CVD) that is deserving of more clinical attention. The cardiovascular community has responded with heightened awareness and interest. ATP III criteria for metabolic syndrome differ somewhat from those of other organizations. Consequently, the National Heart, Lung, and Blood Institute, in collaboration with the American Heart Association, convened a conference to examine scientific issues related to definition of the metabolic syndrome. The scientific evidence related to definition was reviewed and considered from several perspectives: (1) major clinical outcomes, (2) metabolic components, (3) pathogenesis, (4) clinical criteria for diagnosis, (5) risk for clinical outcomes, and (6) therapeutic interventions.
ATP III viewed CVD as the primary clinical outcome of metabolic syndrome. Most individuals who develop CVD have multiple risk factors. In 1988, Reaven2 noted that several risk factors (eg, dyslipidemia, hypertension, hyperglycemia) commonly cluster together. This clustering he called Syndrome X , and he recognized it as a multiplex risk factor for CVD. Reaven and subsequently others postulated that insulin resistance underlies Syndrome X (hence the commonly used term insulin resistance syndrome ). Other researchers use the term metabolic syndrome for this clustering of metabolic risk factors. ATP III used this alternative term. It avoids the implication that insulin resistance is the primary or only cause of associated risk factors. Although ATP III identified CVD as the primary clinical outcome of the metabolic syndrome, most people with this syndrome have insulin resistance, which confers increased risk for type 2 diabetes. When diabetes becomes clinically apparent, CVD risk rises sharply. Beyond CVD and type 2 diabetes, individuals with metabolic syndrome seemingly are susceptible to other conditions, notably polycystic ovary syndrome, fatty liver, cholesterol gallstones, asthma, sleep disturbances, and some …
Obesity is a multifactorial chronic disease characterized by an accumulation of visceral and subcutaneous fat, which leads to a predisposition toward cardiometabolic diseases. A plethora of mechanisms, including abnormalities in lipid metabolism, insulin resistance, inflammation, endothelial dysfunction, adipokine imbalance, and inflammasome activation have been suggested to underlie the relationship between obesity and atherosclerosis. More recent data point toward an emerging role of impaired autophagy and altered gut microbiome homeostasis as potentially contributing factors. This review provides an overview of this area.
Copyright © 2015 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.
Obesity is frequently associated with chronic inflammation, metabolic and vascular alterations which predispose to the development of the Metabolic Syndrome (MetS). However, the individual obesity-related risk for the MetS is not determined by increased fat mass alone. Heterogeneity of body composition, fat distribution and adipose tissue (AT) function may underly the variable risk to develop metabolic and cardiovascular diseases associated with increased body fat mass. Importantly, an inability to increase AT mass by adipocyte hyperplasia may lead to adipocyte hypertrophy and could induce dysfunction of adipose tissue characterized by decreased insulin sensitivity, hypoxia, increased parameters of intracellular stress, increased autophagy and apoptosis and tissue inflammation. As a result, adipocytes and other AT cells release signals (e.g. adipokines, cells, metabolites) resulting in a proinflammatory, diabetogenic and atherogenic serum profile. These adverse signals may contribute to further AT inflammation and secondary organ damage in target tissues such as liver, brain, endothelium, vasculature, endocrine organs and skeletal muscle. Recently, a specific adipocyte volume threshold has been shown to predict the risk for obesity-associated type 2 diabetes.Most likely, impaired adipocyte function is caused by genetic, behavioural and environmental factors which are not entirely understood. Elucidating the mechanisms of adipocyte dysfunction may lead to the identification of novel treatment targets for obesity and the MetS.
Background:
Recent trials of fish oil for the prevention of atrial fibrillation (AF) recurrence have provided mixed results. Notable uncertainties in the existing evidence base include the roles of high-dose fish oil, inflammation, and oxidative stress in patients with paroxysmal or persistent AF not receiving conventional antiarrhythmic (AA) therapy.
Objectives:
The aim of this study was to evaluate the influence of high-dose fish oil on AF recurrence, inflammation, and oxidative stress parameters.
Methods:
We performed a double-blind, randomized, placebo-controlled, parallel-arm study in 337 patients with symptomatic paroxysmal or persistent AF within 6 months of enrollment. Patients were randomized to fish oil (4 g/day) or placebo and followed, on average, for 271 ± 129 days.
Results:
The primary endpoint was time to first symptomatic or asymptomatic AF recurrence lasting >30 s. Secondary endpoints were high-sensitivity C-reactive protein (hs-CRP) and myeloperoxidase (MPO). The primary endpoint occurred in 64.1% of patients in the fish oil arm and 63.2% of patients in the placebo arm (hazard ratio: 1.10; 95% confidence interval: 0.84 to 1.45; p = 0.48). hs-CRP and MPO were within normal limits at baseline and decreased to a similar degree at 6 months (Δhs-CRP, 11% vs. -11%; ΔMPO, -5% vs. -9% for fish oil vs. placebo, respectively; p value for interaction = NS).
Conclusions:
High-dose fish oil does not reduce AF recurrence in patients with a history of AF not receiving conventional AA therapy. Furthermore, fish oil does not reduce inflammation or oxidative stress markers in this population, which may explain its lack of efficacy. (Multi-center Study to Evaluate the Effect of N-3 Fatty Acids [OMEGA-3] on Arrhythmia Recurrence in Atrial Fibrillation [AFFORD]; NCT01235130).
During the 1970s, 2 Danish investigators, Bang and Dyerberg, on being informed that the Greenland Eskimos had a low prevalence of coronary artery disease (CAD) set out to study the diet of this population. Bang and Dyerberg described the "Eskimo diet" as consisting of large amounts of seal and whale blubber (ie, fats of animal origin) and suggested that this diet was a key factor in the alleged low incidence of CAD. This was the beginning of a proliferation of studies that focused on the cardioprotective effects of the "Eskimo diet." In view of data, which accumulated on this topic during the past 40 years, we conducted a review of published literature to examine whether mortality and morbidity due to CAD are indeed lower in Eskimo/Inuit populations compared with their Caucasian counterparts. Most studies found that the Greenland Eskimos and the Canadian and Alaskan Inuit have CAD as often as the non-Eskimo populations. Notably, Bang and Dyerberg's studies from the 1970s did not investigate the prevalence of CAD i