Molecular Nutrition & Food Research

This study examined the effects of administering the probiotic Lactiplantibacillus plantarum Probio87 on the vaginal microbiota of HPV‐positive women, highlighting alterations in bacterial and fungal communities and their potential influence on vaginal and overall health. In a double‐blind, randomized, placebo‐controlled study, participants consumed daily doses of Probio87 (1 × 10⁹ CFU/sachet) or a placebo for 12 weeks. Vaginal swabs were collected, and DNA was extracted for 16S rRNA and the internal transcribed spacer (ITS) region amplification via PCR, followed by sequencing of bacterial and fungal microbiota. The probiotic group showed improved alpha and beta diversity, with an increase in beneficial Lactobacillus (p = 0.014) and Phascolarctobacterium faecium (p = 0.041), while decreasing the abundance of pathogens like Streptococcus and Candida (p = 0.011). Additionally, vaginal health questionnaires linked probiotic use to improved vaginal and mental health in HPV‐positive women. L. plantarum Probio87 demonstrated clinical and psychological benefits in HPV‐positive women by balancing the vaginal microbiome, reducing pathogenic species, and promoting the growth of beneficial microorganisms.

Polycystic ovary syndrome (PCOS) is a common endocrine disorder that affects metabolic and reproductive health in women. α‐Linolenic acid (ALA)–rich flaxseed oil as a dietary food has been suggested to offer potential therapeutic benefits in managing metabolic disturbances associated with PCOS. This study investigates the effects of ALA‐rich flaxseed oil on lipid metabolism and gut microecology in a PCOS rat model. The PCOS model was induced in rats using letrozole, and the animals were then administered ALA‐rich flaxseed oil. Metabolomics, transcriptomics, 16S rRNA sequencing, hormonal levels, and markers of metabolic health were assessed. Results showed that ALA‐rich flaxseed oil significantly improved lipid metabolism by reducing serum cholesterol and triglycerides. In addition, we found that the improvement in lipid metabolism may be associated with the activation of the GPR120‐cAMP pathway. Furthermore, gut microbiota analysis revealed a restoration of gut microbial ecology, with a shift toward a more balanced and healthy microbial composition. ALA‐rich flaxseed oil shows promising potential as a dietary intervention for managing metabolic disturbances in PCOS. Its effects on lipid metabolism and gut microecology highlight its nutritional relevance, offering new insights into the dietary management of PCOS and its associated metabolic disorders.

This study investigates the influence of phytic acid on Fe and Zn bioaccessibility and impact of phenolics on free radical scavenging activity in 13 diverse pearl millet (PM) genotypes. Forty‐three phenolic compounds were identified using UPLC‐(ESI)‐QToF‐MS. Free (173.01–217.11 mg GAE/100 g), bound (102.97–142.52 mg GAE/100 g), and total phenolic content (286.04–337.63 mg GAE/100 g) varied significantly among genotypes. Phenolic content positively correlated with radical scavenging activity (36.43%–47.56%, DPPH assay). INFOGEST in vitro digestion showed increasing phenolic bioaccessibility from oral (12.58%–23.55%) to gastric (48.4%–72.25%) to intestinal (67.17%–90.26%) phases. Bioaccessibility of Fe (10.55%–14.46%) and Zn (13.48%–19.79%) was negatively correlated with phytic acid (629.02–797.71 mg/100 g) content. WGI 100, with the lowest phytic acid content, had the highest bioaccessibility, whereas Dedha Bajra, with the highest phytic acid content, had the lowest bioaccessibility of Fe and Zn recorded. PM genotypes are rich in phenolics, having high radical scavenging potential. However, higher phytic acid content reduced Fe and Zn bioaccessibility, reinforcing its antinutritional effect on mineral bioavailability.

This study aimed to determine the associations between sulfur microbial diet (SMD) and all‐cause, cardiovascular disease, and cancer mortality. A total of 91 891 adults were included from the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. To evaluate adherence to this dietary pattern, the SMD score was calculated with higher scores indicating greater compliance. The hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using the Cox proportional hazards regression. After a median follow‐up of 15.0 years, 20 706 all‐cause deaths were noted. The participants in the highest quartile of the SMD score had an enhanced risk of death from all causes (HR: 1.12, 95% CI: 1.07, 1.17) and cancer (HR: 1.15, 95% CI: 1.06, 1.24) than those in the lowest quartile. Dose–response analysis indicated a nonlinear association between the SMD score and both all‐cause and cancer mortality. Subgroup analyses demonstrated a significant positive association between the SMD score and all‐cause mortality in participants aged 65 years and older. Higher adherence to the SMD is linked to increased risks of all‐cause and cancer mortality in the US population. These study findings suggest that intestinal sulfur‐metabolizing bacteria may play a role in the association between diet and health outcomes.

Obesity‐induced mitochondrial dysfunction impairs skeletal muscle metabolic flexibility. Gallic acid possesses the ability to modulate metabolic homeostasis. This study aimed to investigate the impact of gallic acid on high‐fat diet (HFD)‐induced metabolic disorders in skeletal muscle. Twenty‐four mice were randomly divided into three groups and subjected to HFD and gallic acid intervention for 12 weeks. The overall glycolipid metabolic status, exercise performance, muscle fiber type, and antioxidant capacity of skeletal muscle in HFD‐fed mice treated with gallic acid were assessed. Untargeted metabolomics analysis was performed to evaluate key metabolic characteristics in skeletal muscle. Gallic acid administration effectively reduced fat accumulation, improved exercise capacity, and enhanced antioxidant capacity in HFD‐fed mice. Untargeted metabolomics revealed that gallic acid positively regulated lactate metabolism and mitochondrial fatty acid oxidation. Mechanistically, gallic acid intervention increased fatty acid oxidation capacity while inhibiting lactate production and mitochondrial protein lactylation in skeletal muscle. Moreover, the role of gallic acid in enhancing mitochondrial function through the LDHA‐lactate axis has been demonstrated in C2C12 cells. Collectively, gallic acid ameliorated HFD‐induced metabolic disorders in skeletal muscle, indicating a novel role for gallic acid in ameliorating diet‐induced skeletal muscle metabolic disorders by regulating lactate metabolism and mitochondrial function.

Since our previous studies found a low‐carbohydrate (CHO) diet containing soy protein and fish oil (i.e., 15%Amylose/Soy/FO) significantly reduced tobacco carcinogen‐induced lung nodules in A/J mice, breast tumors in C3(1)/Tag mice, and myelomalignancy in miR‐146a knockout mice, we asked herein if this CHO diet could also reduce colorectal cancer. We tested the efficacy of the 15%Amylose/Soy/FO diet in preventing colitis‐induced colorectal cancer using an azoxymethane/dextran sodium sulfate BALB/c mouse model. The 15%Amylose/Soy/FO diet significantly reduced colon tumor numbers compared to a Western diet and this was associated with a reduction in blood glucose, and a trend towards an increase in plasma β‐hydroxybutyrate and an increase in liver fatty acid synthase, suggesting a systemic metabolic shift from glucose to fatty acids as an energy source. In addition, our CHO diet reduced proinflammatory cytokines, induced a marked change in the fecal microbiome, an increase in cecal and fecal acetate, and a reduction in interleukin‐17A expressing cells in the colonic tumors of mice on the 15%Amylose/Soy/FO diet. Taken together, our results suggest the 15%Amylose/Soy/FO diet ameliorates colitis and prevents the subsequent development of colorectal cancer, in part by an acetate‐mediated reduction in TH17 cell development.

Chitosan is suggested to have prebiotic properties, yet clinical evidence on its in vivo effects on the human gut microbiota and various health factors remains scarce. This study aimed to evaluate the effects of chitosan supplementation on gut microbiota composition and various health factors in Icelandic females. Sixty Icelandic females (aged 26–70; BMI 19.1–35.0 kg/m²) were randomized to a 12‐week intervention receiving either 3 g/day of encapsulated chitosan (LipoSan Ultra) (TRG, n = 28) or placebo (PLG, n = 32). Anthropometrics, health factors, endurance, and health status questionnaires were collected at baseline (T1) and post‐intervention (T3). All values remained within reference ranges at both timepoints in both groups, except weight, waist circumference, and fat mass, which were above. In TRG, alkaline phosphatase (ALP) levels increased, and fecal consistency shifted toward constipation. 16S rRNA microbial analysis showed decreased diversity/evenness, increased T1–T3 separation by nonmetric multidimensional scaling, and higher Actinobacteriota abundance. Genus level shifts included reduced Blautia, Eubacterium hallii, CAG‐56 levels and increased Ruminococcus gnavus, Clostridium innocuum, Bifidobacterium, and Holdemania. This novel clinical study demonstrates that 12 weeks of chitosan supplementation alters gut microbiota composition without affecting general health status in females. Trial Registration This trial was registered at Clinicaltrials.gov as NCT04551365

Scope Carbohydrate intake profoundly shapes hepatic metabolism, impacting crucial pathways like glycolysis, lipogenesis, and ketogenesis. This study aimed to investigate the effects of carbohydrate deprivation on hepatic glycolipid metabolism in mice. Methods & Results Male C57BL/6J mice were subjected to a 4‐week dietary intervention where they were assigned to one of four groups: standard diet (CON), low‐carbohydrate high‐fat diet (LCD), no‐carbohydrate high‐fat diet (NCD), and high‐carbohydrate no‐fat diet (HCD). Post‐intervention analysis revealed that the NCD group exhibited reduced blood glucose, HbA1c, and LDL‐C levels compared to the CON group. Additionally, the NCD group showed decreased liver glycogen content and liver index. Histopathological examination of liver sections indicated less lipid accumulation and a significant down‐regulation of hepatic de novo lipogenesis (DNL)‐related proteins in the NCD group. Metabolomics analysis demonstrated higher hepatic acylcarnitine levels and lower lysophosphatidylcholine and fatty acyl metabolites levels in the NCD group. Furthermore, protein expression levels of pAMPK, pHSL, PGC1α, CPT1A, and OXPHOS were elevated in the NCD group, suggesting enhanced hepatic energy metabolism and lipolysis ability. Conclusion These findings suggested that carbohydrate deprivation enhances fatty acid metabolism capacity and inhibits lipogenesis via the AMPK/PGC1α pathway to improve glucose and lipid metabolism in mice.

The first 6 months of life are crucial for an infant's growth and gastrointestinal development. Proper nutrition is vital to support this maturation, especially considering the limited digestive capacity of infants at this stage. While breast milk is considered the optimal source, infant formula serves as an important alternative for mothers who cannot breastfeed. This study employed human embryonic stem cell‐derived small intestinal organoids (SIOs) to simulate neonatal intestinal digestion and nutrient absorption. Breast milk and different brands of infant formulas were subjected to in vitro digestion and subsequent SIO absorption. Metabolomics analysis was conducted at three stages: predigestion, postdigestion, and postabsorption. Significant differences were found in the metabolic profiles between breast milk and infant formulas at each developmental stage, indicating distinct nutrient processing and absorption patterns. The study highlights the metabolic and absorption variations between breast milk and formula during early infancy. These findings provide important insights into how different nutritional sources influence gastrointestinal development, offering valuable guidance for optimizing infant formula composition to better replicate the benefits of breast milk.

Scope This study investigated the limited epidemiological data for Koreans regarding the impact of meat intake on metabolic dysfunction‐associated steatotic liver disease (MASLD), a growing diet‐influenced health concern. We investigated sex‐specific associations of red meat, poultry, and processed meat consumption with MASLD risk using data from the Korean Genome and Epidemiology Study. Methods and results The study followed 46 296 participants from the Health Examinees cohort of the Korean Genome and Epidemiology Study, utilizing a validated 106‐item food‐frequency questionnaire to estimate meat intake. Cox proportional hazard models, adjusted for confounders, were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for MASLD risk. The high total meat intake significantly increased MASLD risk by 40% in men (HR 1.40; 95% CI 1.09–1.80) and 52% in women (HR 1.52; 95% CI 1.18–1.96). Red meat consumption elevated risk by 34% in men (HR 1.34; 95% CI 1.04–1.73) and 43% in women (HR 1.43; 95% CI 1.12–1.83). Processed meat intake also increased risk by 32% in men (HR 1.32; 95% CI 1.12–1.55) and 50% in women (HR 1.50; 95% CI 1.23–1.82). Conclusion The findings indicate that red and processed meat consumption substantially elevates MASLD risk in Koreans.

Fructose is a nutrient used widely and indiscriminately as a sweetener in various types of foods and beverages. Accumulating evidence suggests that dietary fructose has a close relationship with metabolic diseases like hyperuricemia (HUA). However, the role and metabolic fate of fructose intake remain elusively obscure. The present work made a pioneering endeavor to unravel the potential mechanistic link between prolonged fructose overconsumption and the incidence of HUA. High‐fructose (30%) free drinking was provided to rats for 17 weeks. Results indicated that long‐term high‐fructose intake remarkably increased the levels of uric acid, creatinine, and urea. Besides, mild renal alteration induced by high fructose was observed in the hyperuricemic rats. Instead of activating ketohexokinase, high‐fructose intake activated the pentose phosphate pathway (PPP) to produce abundant ribose 5‐phosphate and phosphoribosyl pyrophosphate. The de novo purine biosynthesis (DNPB) was activated to produce purines and accelerate the purine cycle. High‐fructose intake significantly enhanced the expression of core enzymes of DNPB and changed the purinosome formation and forming areas. Furthermore, up‐regulation of xanthine oxidase (XOD) promoted the purine metabolism, resulting in increased levels of inosine monophosphate, inosine, hypoxanthine, and xanthine. Besides, the targeted metabolome analysis also showed that fructose metabolism triggered bioenergetic alteration with the consumption of ATP and a surge in NAD⁺ and NADH. Hence, chronic ingestion of high‐fructose contributed to HUA, which was intimately associated with activation of original biosynthetic and metabolic pathways of endogenous purine simultaneously mediated by PPP, DNPB, and XOD and accompanied by bioenergetic alteration.

Corn silk, the stigmas and styles of maize, is a traditional medicinal herb with promising anti‐aging potential. This review systematically examines its bioactive compounds, including flavonoids, polysaccharides, terpenoids, and sterols, which contribute to its antioxidant, anti‐inflammatory, anti‐tumor, and metabolic regulatory effects. These properties support its potential therapeutic applications in aging‐related conditions such as neurodegenerative diseases (e.g., Alzheimer's and Parkinson's), cardiovascular disorders, metabolic diseases (e.g., diabetes and obesity), and kidney dysfunction. Preclinical studies highlight corn silk's role in mitigating oxidative stress and inflammation—key drivers of aging. Additionally, preliminary clinical trials, particularly on its anti‐diabetic effects, show promise, but larger randomized controlled trials are needed to establish its safety and efficacy. Future research should focus on standardizing extraction methods, elucidating mechanisms of action, and exploring synergistic interactions among its bioactive constituents. Together, this review emphasizes the need for continued investigation into corn silk as a natural, multi‐target therapeutic agent for aging and age‐related diseases, and advancing its potential for clinical applications.

Patients with stage II‐III colorectal cancer (CRC) often receive fluoropyrimidine‐based chemotherapy, usually combined with other regimens, of which ∼50% experience severe chemotherapy‐induced toxicities. The B‐vitamin folate has been associated with toxicity risk, possibly through effects on DNA methylation. Here, we examined the potential role of folate‐associated DNA methylation in the context of chemotherapy‐induced toxicities. Systematic literature searches were conducted to identify studies investigating either DNA methylation profiles associated with folate status/intake or with toxicities. Overlapping CpG sites and genes across studies investigating associations for “folate‐DNA methylation” and “DNA methylation‐toxicities” were identified. The probability of overlap was tested using hypergeometric tests and Gene Ontology and KEGG pathway analyses were performed. Six studies were included. A significant number of CpGs and genes overlapped with altered methylation in response to both folate and hand‐foot syndrome (HFS) or thrombocytopenia. Moreover, methylation of genes within the KEGG pathway “focal adhesion” was related to folate status/intake and occurrence of HFS, thrombocytopenia, and neutropenia. We identified some overlapping DNA methylation profiles related to both folate exposures and toxicities. This provides preliminary evidence implying folate‐associated DNA methylation may determine risk of toxicities, and therefore may be considered a modifiable factor for improving patient outcomes.

Metabolic disturbances in late gestation contributes to oxidative stress and mitochondrial dysfunction in the placenta, leading to intrauterine growth retardation (IUGR), all of which are associated with reduced nicotinamide adenine dinucleotide (NAD⁺) levels. This study aimed to investigate the effects of maternal supplementation of β‐nicotinamide mononucleotide (NMN), a nutraceutical NAD⁺ precursor, on IUGR rate and its underlying mechanisms. A total of 24 sows were randomly divided into either the control or NMN group, with each sow in the NMN group receiving 0.2 g of NMN per day. The results demonstrated that NMN supplementation significantly reduced the IUGR rate and increased NAD⁺ levels in the placenta of sows. Furthermore, NMN supplements upregulated mRNA and protein expressions of key mitochondrial regulators, such as PGC‐1α, declined oxidative stress and apoptosis, and improved lipid metabolism in the placenta. These effects were linked to the upregulation of p‐AMPK and the downregulation expression of p‐mTOR. Taken together, this study indicates that maternal NMN supplementation reduces the IUGR rate by improving mitochondria function, enhancing lipid metabolism, and declining oxidative stress in the placenta.

Aligned with the principles of the circular bioeconomy, this study explores the use of winemaking by‐products as a source of bioactive phenolic compounds. Skins and seeds from Tempranillo and Graciano grapevine varieties were conditioned to prepare a phenolic‐rich beverage. To study its hypoglycemic properties, a pilot trial was conducted to evaluate postprandial glycemia after the intake of the wine by‐product‐based beverage (WBB). The postprandial glycemia of 10 healthy adults was measured after the intake of: (i) water + sugar solution, (ii) WBB + sugar solution, and (iii) WBB + water. In parallel to blood glucose measurement, blood samples were also collected using dried blood spot cards to determine the phenolic metabolites by UHPLC‐QqQ‐MS/MS. Although blood glucose levels tended to decrease after WBB intervention, these changes were not statistically significant related to the interindividual variability. The volunteers showing a reduction in blood glucose were classified as “responders”, and those who showed no changes were classified as “non‐responders”. Wine by‐products can be effectively used in functional beverages formulation to increase bioactive compound content and manage postprandial glucose in some individuals.

This study investigated the photoperiod‐dependent effects of eight phenolic‐enriched fruit extracts on postprandial blood triacylglyceride (TAG) levels and serum cytokine and CRP levels in F344 rats after an oral lipid tolerance test (OLTT) and lipopolysaccharide (LPS)–induced inflammatory challenge, respectively. Animals were exposed to short (6‐h light, L6) or long (18‐h light, L18) photoperiods and orally supplemented with fruit extracts (100 mg/kg) for 2 weeks. Extracts were obtained from seasonal fruits (cherries, plums, apricots, strawberries, persimmon kakis, grapes, oranges, and pomegranates). Temporal homeostasis disruption was induced by an OLTT and LPS challenge. No differences in blood postprandial TAG levels were observed in the L6‐ and L12‐control groups. However, in the experimental groups, the postprandial TAG response depended on the photoperiod and fruit extract consumption, mainly cherry and plum extracts in L6 (p < 0.05). In addition, control rats exposed to L6 exhibited higher blood IL‐6 and TNF‐α levels after inducing LPS‐inflammatory response. Notably, winter‐fruit and strawberry extracts were the most efficient at lowering proinflammatory cytokines. These findings show the effectiveness of specific fruit extracts in modulating postprandial TAG levels and acute inflammatory responses, being their effects photoperiod‐dependent, opening the door to the design of functional ingredients specific for each season.

In the present study, we investigated the potential biological effects of proteins and peptides extracted from four different commercial quinoa grain varieties: Black (B), Red (R), White (W), and Royal White (RO), using Caco‐2 cells as a proliferation model. Concentration–response curves were constructed to evaluate cytotoxicity and antiproliferative effects. Interestingly, peptides exhibited higher cytotoxicity than proteins, particularly in R and RO quinoa varieties. Based on these findings, we used a data mining approach to identify and compare the cytotoxic proteins in the four quinoa varieties. Using their relative abundance, we successfully classified R and RO quinoa as a cohesive group using classification models. To gain deeper insights into the biological effects on cells, we comprehensively analyzed the differential expression of apoptosis biomarkers using liquid chromatography‐tandem mass spectrometry (LC‐MS/MS) targeted proteomics. Finally, we correlated the apoptosis profile with the relative abundance of cytotoxic proteins. All these studies were supported by the application of multivariate data analysis. The results demonstrated the potential anticancer of quinoa grain proteins and peptides and provided the basis for more focused mechanistic studies aimed at developing functional foods and nutraceuticals.

Efficient and stable animal models of celiac disease (CD) are crucial for CD research, dietary supplement research, and new drug development. This study aimed to establish CD models by administering gliadin to parental mice and first‐generation mice on gluten‐free diets using two ways: intraperitoneal injection and a combination of sensitization of intraperitoneal injection and gavage. Various indicators, including clinical manifestations, characteristic indicators of CD, inflammatory factors, intestinal barriers, immune cells, and other related indicators, were used to compare different modeling methods. The results showed that all four methods could induce varying degrees of CD symptoms in mice. Additionally, intraperitoneal injection of gliadin was more effective than the combination sensitization, and first‐generation mice on gluten‐free diets exhibited more significant CD symptoms compared to parental mice. The analysis revealed that intraperitoneal injection in first‐generation mice led to significant increases in specific IgG and total IgE antibody levels (p < 0.01); a marked shortening of intestinal villus and crypt hyperplasia in the jejunum; significant increases in pro‐inflammatory factors IFN‐γ, TNF‐α, IL‐17, and IL‐15 (p < 0.01); and a significant decrease in the anti‐inflammatory factor IL‐4 (p < 0.01). Additionally, there was a severe imbalance of immune cells in the spleen and intestinal lymph nodes. These results suggest that the model of intraperitoneal injection in first‐generation mice was more efficient, stable, and significant in the construction. This study provides a theoretical basis for the efficient construction of CD models. image

Dietary fiber, especially resistant starch (RS) Type 2 (RS2) found in high‐amylose maize starch (HAMS), is vital for gut health and helps prevent colon cancer. In contrast to most nutrients, dietary fiber is not degraded by the intestinal enzymes; it reaches the distal parts of the gut, where it is fermented by the gut microbiota into short‐chain fatty acids (SCFAs), such as acetate, propionate, and butyrate. SCFAs energize colonocytes, reduce inflammation, and enhance gut immunity. HAMS is absorbed in the colon, where it ferments to create SCFAs that feed good gut flora and have antiinflammatory and antiproliferative effects. RS2 in HAMS modulates gene signaling, activates tumor‐suppressor genes like tumor suppressor protein (p53), exhibits antidiabetic, cholesterol‐lowering, and antiinflammatory effects. Incorporation of RS2‐rich sources enhances gut barriers, decreases colorectal cancer biomarkers, and counteracts the negative impacts of low‐fiber Western diets, making HAMS a promising functional food for chronic disease prevention and health promotion.

Lipid oxidation can induce liver oxidative stress and lipotoxic damage, while selenium (Se) possesses detoxification, antioxidation, immunity, and liver protection functions. However, the effects of Se and oxidized lipids on liver oxidative stress and lipid metabolism, along with the underlying mechanisms, remain underexplored. This study aimed to investigate the protective effects of Se against liver injury induced by oxidized soybean oil (OSO) in mice. C57BL/6J mice (n = 60) were randomly divided into Control (0.2 mg/kg Se+7% fresh soybean oil), OSO (0.2 mg/kg Se+7% OSO), and OSO+Se (1.0 mg/kg Se+7% OSO) groups for 10 weeks. The results showed that Se supplementation mitigated the morphological structure and functional impairment, inflammation, and oxidative stress of the liver caused by OSO, and improved changes to the liver fatty acid profile and lipid metabolism disorders. It also reversed the OSO‐induced imbalance of liver polyunsaturated fatty acid metabolites and inhibited OSO‐induced activation of the PI3K‐AKT pathway. Se may activate the Nrf2 pathway and inhibit the PI3K‐AKT pathway to improve inflammation, oxidative stress, and fatty acid metabolism disorders, thereby reducing liver injury. These findings highlight the nutritional relevance of Se as a potential therapeutic agent for preventing liver damage from oxidized lipids.

Trimethylamine N ‐oxide (TMAO) is a uremic toxin accumulated in patients with chronic kidney disease (CKD) and involved with atherosclerosis. TMAO is derived from the gut microbiota (nutrient fermentation) and is found in some fish and seafood. This pilot study evaluated the acute effects of cod fish, red meat, and vegetable meal consumption on plasma TMAO levels in nondialysis CKD patients. Patients (five women, three men, 72.5 [7.7] years, body mass index [BMI], 25.6 [1.4] kg/m ² , glomerular filtration rate, 32.5 [18.5] mL/min) consumed lunches containing codfish, red meat, and chickpeas, within a 7‐day interval between meals. TMAO plasma levels were assessed using the HPLC‐EM/EM method before and after the 4‐h meal challenge. Patients presented TMAO plasma levels of 9.06 µM. Consumption of codfish significantly increases the TMAO levels (to 23.5 µM, p < 0.001) compared to red meat and chickpeas. We conclude that codfish, compared to red meat and vegetable meal, provoked a transient elevation in TMAO levels in patients with CKD. Therefore, this result suggests that it is prudent to prescribe fish with low TMAO content for these patients. The response to ingesting TMAO‐rich foods in CKD patients needs more study.

Ischemic stroke leads to significant neurological deficits and remains a leading cause of disability and mortality worldwide. β‐1,3‐glucans‐rich Euglena gracilis (EG), a type of dietary supplement, was reported to regulate metabolic perturbation and the gut‐brain axis that have been implicated in aggravation of the disease. The present study aimed to investigate the neuroprotective effects of EG supplementation in an ischemic stroke model in middle‐aged mice fed with a high‐fat high‐fructose (HFHF) diet. The mice were divided into three groups: HFHF, HFHF+EG (HFHF_EG), and HFHF+Sham (HFHF_Sham). After 8 weeks of dietary intervention, ischemic stroke was induced via middle cerebral artery occlusion (MCAO) in the HFHF and HFHF_EG groups. The data revealed that EG supplementation significantly reduced infarct volume, alleviated neurological deficits, and enhanced synaptic plasticity in the hippocampus. The neuroprotective effects of EG were associated with improved intestinal barrier integrity, reduced systemic and neuroinflammation, and modulation of the hippocampal insulin signaling pathway. Furthermore, EG supplementation favorably altered gut microbiota composition, especially enhancing the relative abundance of beneficial bacteria and short‐chain fatty acid production. Our results suggest that EG supplementation may be a promising dietary strategy to mitigate HFHF diet‐induced exacerbation of ischemic stroke via the gut‐brain axis.

Opuntia ficus‐indica (OFI) has attracted much attention as a source of antioxidant and antiinflammatory compounds. We hypothesize that the antioxidant content of OFI cladode extract may improve adipocyte dysfunction resulting from inflammatory stimulation of hypertrophic adipocytes. To this end, the properties of OFI cladode hydroalcoholic extract were evaluated in terms of antioxidant activity, regulation of adipocyte inflammation, and adipocyte/monocyte interaction in human adipocytes rendered dysfunctional by the proinflammatory cytokine tumor necrosis factor‐α (TNF‐α). The major phenolic compounds identified were isorhamnetin derivatives and phenolic acids, including piscidic and eucomic acids. Our results show that OFI cladode extract exhibits antiradical activities and reduces the adhesion and transmigration activity of monocytes to inflamed adipocytes by inhibiting various cytokines, chemokines, and adhesion molecules such as interleukin (IL)‐6 and IL‐8 by ∼80%, monocyte chemotactic protein (MCP)‐1, C‐X‐C motif chemokine ligand (CXC‐L)10, macrophage colony‐stimulating factor (M‐CSF) from 40% to 50%, and intercellular adhesion molecule‐1 (ICAM‐1) by 70% at the higher concentration. In structurally and mechanistically by protein–ligand docking profiling study, piscidic acid proved to be the best potential candidate for a regulatory interaction with the activities of nuclear factor erythroid 2‐related factor 2 (NRF‐2) and nuclear factor‐κB (NF‐κB). In summary, these data highlight the potential of OFI as a dietary supplement in nutritional treatments aimed at combating the inflammatory stigmata of obesity.

Targeting angiogenesis as a strategy for treating cancer or vascular‐associated complications is an inspiring field for many investigators. An active area within this discipline is the search for agents capable of modulating angiogenesis in order to ameliorate its structural and functional abnormalities associated with these diseases. (Poly)phenols are a broad group of molecules, many of which fall within the category of natural compounds with therapeutic potential. These potential medicinal effects have launched a considerable number of studies investigating the pro‐ and(or) anti‐angiogenic properties of (poly)phenols in different (patho)physiological settings. The purpose of this review is to summarize the current evidence of the role of (poly)phenols in modulating angiogenesis. This review will guide the reader through preclinical and human investigations describing the pro‐ and anti‐angiogenic effects of these compounds in different pathophysiological context, the cellular and molecular mechanisms associated, the key points in the design and evaluation of the effects described, and suggest new approaches to be considered in future studies to overcome the current limitations.