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Parallel epidemic of diabetes and sugar consumption. Sugar intake has been increasing steadily over the last 200 yr (33, 310, 318 –319). In parallel, there has been a rise in diabetes (first described based on death certificates of diabetes-related deaths per 100,000 population) (4) and later by diabetes prevalence rates (268). The data showing sugar consumption are adapted with permission from R.J. Johnson, et al.: Am J Clin Nutr 86:899 –906, 2007 (27) © The American Society for Nutrition.
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We propose that excessive fructose intake (>50 g/d) may be one of the underlying etiologies of metabolic syndrome and type 2 diabetes. The primary sources of fructose are sugar (sucrose) and high fructose corn syrup. First, fructose intake correlates closely with the rate of diabetes worldwide. Second, unlike other sugars, the ingestion of excessiv...
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The intake of added sugars, such as from table sugar (sucrose) and high-fructose corn syrup has increased dramatically in the last hundred years and correlates closely with the rise in obesity, metabolic syndrome, and diabetes. Fructose is a major component of added sugars and is distinct from other sugars in its ability to cause intracellular ATP...
Excessive consumption of diets high in sugars and saturated fat, frequently known as western diet (WD), may lead to obesity and metabolic syndrome. Recent evidence shows that WD-induced obesity impairs cardiac function, but the underlying mechanisms are not fully understood. Trimethylamine N-oxide (TMAO), a gut microbiota-dependent metabolite of sp...
Fructose-containing added sugars, such as sucrose and high-fructose corn syrup, have been experimentally, epidemiologically, and clinically shown to be involved in the current epidemics of obesity and diabetes. Here we track this history of intake of sugar as it relates to these epidemics. Key experimental studies that have identified mechanisms by...
The objective of the current study was to explore our hypothesis that average consumption of fructose and fructose containing sugars would not increase risk factors for cardiovascular disease (CVD) and the metabolic syndrome (MetS). A randomized, double blind, parallel group study was conducted where 267 individuals with BMI between 23 and 35 kg/m²...
Fructose is a sweet tasting sugar that is found naturally in fruits and some vegetables and has been part of the human diet—in modest amounts—for eons. The increasing consumption of sugar has dramatically increased our exposure to fructose (1). Sugar consumption has risen more than 40-fold since the Declaration of Independence was signed 250 years...
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... Fructose metabolism increases uric acid production, which inhibits endothelial nitric oxide, contributing to hypertension, insulin resistance, and weight gain [15]. A daily fructose intake exceeding 50 g may contribute to metabolic syndrome and T2DM development by elevating circulating uric acid levels and promoting intracellular fat accumulation in the liver, brain, blood vessels, muscles, kidneys, and adipose tissue [16,17]. ...
Background: Fructose (50% of sucrose/sugar) is one component of free-sugars and is metabolized to uric acid, which is a known risk factor for gout and metabolic syndrome. Pacific peoples in New Zealand experience a higher prevalence of gout, type 2 diabetes, and overweight/obesity than other ethnic groups. Interestingly, despite having a similar body mass index (BMI), they tend to have a higher proportion of appendicular skeletal muscle mass (ASMM) and less fat than other ethnic groups. Given this context, this study aimed to evaluate the associations between serum uric acid (SUA), free-sugar intake, and ASMM. Methods: In a nested sub-study from the Pacific Islands Families birth-cohort study, 101 boys and 99 girls (all aged 14 and 15 years) self-reported how often they had consumed foods containing sugar in the past month. Anthropometry, body fatness, and ASMM by dual-energy X-ray absorptiometry and metabolic risk factors, including SUA were measured. Results: Overall, 43% of girls and 57% of boys consumed ‘sugary drinks’ twice or more a day. When analyzed by group, ASMM was positively related to SUA for both boys and girls (r = 0.593, p < 0.0001). The effect of the intake of ‘sugary drinks’ on SUA (r = 0.176, p = 0.013) was reduced when ASMM was considered in the relationships. Conclusions: This study shows high SUA levels in Pacific adolescents, with a positive association between ASMM and SUA in both genders. Sugary drink intake was positively associated with SUA in both boys and girls. High ASMM in Pacific people and an increased risk for raised SUA make it important to work with Pacific communities to reduce added sugar intake and adopt integrated, family-based, culturally centered, and life-course approaches to prevent chronic diseases, including gout.
... Several mechanisms have been hypothesised to be involved in the generation of IR by fructose, including classic mechanisms (adiposity based) and those independent of energy intake or weight gain. Among the latter: direct effects on insulin signalling or on hepatic glucose production, and indirect effects resulting from hepatic and muscle lipid accumulation (58) . For example, excess fructose intake can lead to an increase in de novo lipogenesis in the liver by bypassing the major rate-limiting step of glycolysis at the phosphofructokinase step (30) . ...
A positive association has been demonstrated between consumption of sucrose-sweetened beverages and the prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD). Since the administration of 30% sucrose in the drinking water (SRD) to rats has proven to be a good model of systemic insulin resistance, the aim of our study was to analyze the effect of caloric restriction applied on SRD-treated rats by switching back to a standard diet, on liver morphology, function, and metabolism.
Consumption of a SRD causes a metabolic shift towards gluconeogenesis and fatty acid synthesis leading to an increase in triacilglyceride (TAG) levels in plasma and in the liver that were associated with a decrease in insulin sensitivity. Moreover, our results show that animals fed a SRD develop steatohepatitis characterized by the generation of oxidative stress, endoplasmic reticulum (ER) stress, inflammation, and apoptosis. Although no histological changes were observed after a two-week caloric restriction, key pathways associated with the progression of MASLD as inflammation, ER stress and apoptosis were slowed down. Notably, this two-week intervention also increased liver insulin sensitivity (evaluated by AKT activity in this tissue) and drove the lipid metabolic profile towards oxidation, thus lowering circulating TAG levels.
In summary, the present study uncovers underlying mechanisms affected, and their metabolic consequences, during the first stages of the phenotypic reversal of steatohepatitis by switching back to a standard diet after receiving sucrose-sweetened water for several weeks.
... Tese fndings reveal that the AEMFE possess hematopoietic efect in alloxan-induced T2DM and stabilizing the RBC membrane fragility similar to a previous study on R. serpentine and A. esculentus [15,71]. On the other hand, AEFME also reversed the alloxan-induced increase in WBCs toward normal, which shows the anti-infammatory efect of AEFME [71][72][73]. Te ameliorating efect of AEFME on RBC count and total Hb level further improved the hematological parameters including PCV, MCV, MCH, and MCHC toward normal [71]. Terefore, the AEMFE decreased the occurrence of mild anemia, which usually observed in diabetes [74]. ...
Due to inadequate treatment, diabetes mellitus, which is characterized by hyperglycemia, is a global health challenge that requires creative management techniques. This study explores the therapeutic potential of Abelmoschus esculentus L. Moench fruit extracts in diabetes, offering an ample approach includes phytochemical analysis, qualitative and quantitative assessments, antidiabetic efficacy, antioxidant potential, and in vivo and in vitro investigations. Thin-layer chromatography (TLC), high-performance liquid chromatography (HPLC), and gas chromatography–mass spectrometry (GC–MS) were utilized to disclose the phytochemical profile of the fruit extracts, which indicated a diverse range of bioactive compounds. Four polyphenolic compounds including chlorogenic acid, quercetin, rutin, and morin were confirmed by HPLC fingerprinting, with rutin being the most prevalent. Qualitative analysis reveals the presence of carbohydrates, emodin, terpenoids, lignin, glycosides, and anthraquinones, while indicating the absence of amino acids, anthocyanins, phlobatannins, lactones, and leucoanthocyanins. Quantitative analysis reveals total phenolic, tannin, and flavonoid. In vitro assessments demonstrate the ability of the extracts to inhibit alpha amylase. Radical scavenging activities were evaluated through DPPH assay, underscoring their antioxidant capacity with high effect in methanol extracts. Additionally, the methanol extract decreased the blood glucose level of Type 2 diabetic mice. Notably, test samples stabilized blood glucose levels, reversed deviations in blood profile parameters, blood biochemistry, and regulated organ weight. Based on its antioxidant and antidiabetic effects, as well as positive effects on the physiology of Type 2 diabetic mice, A. esculentus emerges as an important nutraceutical vegetable. As an important nutraceutical vegetable, it holds promise for diabetes management. A. esculentus can be incorporated into dietary interventions for individuals with diabetes, harnessing its natural antioxidant and antidiabetic properties. Our findings validate the traditional use of A. esculentus in green therapeutics. In conclusion, A. esculentus emerges as a valuable ally in the fight against diabetes, bridging the gap between ancient wisdom and modern science. Further research and practical implementation are warranted to fully realize its potential.
... High fructose consumption has been shown to cause insulin resistance in the liver and other tissues, ultimately contributing to obesity [16]. Additionally, the development of visceral fat in the human body poses a significant risk for visceral obesity [14]. ...
Excessive fructose consumption, primarily through processed foods and beverages, has become a significant public health concern due to its association with various metabolic disorders. This review examines the impact of fructose on human health, focusing on its role in obesity, insulin resistance, hyperglycemia, type 2 diabetes, uric acid production, and oxidative stress. Fructose metabolism, distinct from glucose, predominantly occurs in the liver, where it bypasses normal insulin regulation, leading to increased fat synthesis through de novo lipogenesis. This process contributes to the development of non-alcoholic fatty liver disease and elevates the risk of cardiovascular disease. Furthermore, fructose-induced adenosine triphosphate depletion activates purine degradation, increasing uric acid levels and exacerbating hyperuricemia. The overproduction of reactive oxygen species during fructose metabolism also drives oxidative stress, promoting inflammation and cellular damage. By synthesizing recent findings, this review underscores the importance of regulating fructose intake, implementing public health policies, and adopting lifestyle changes to mitigate these adverse effects.
... Since the 1960s, fructose intake increased over time Free sugar: monosaccharides and disaccharides added to foods and beverages by the manufacturer, cook or consumer, and sugars naturally present in honey, sirups, fruit juices and fruit juice concentrates. aHa (Johnson, Perez-Pozo, et al. 2009) adult and Children added sugar < 9 teaspoons, 36 grams, 150 calories for men added sugar < 6 teaspoons, 25 grams, 100 calories for women avoid consuming any added sugar for children < 2 years < 25 grams for children and adolescents Added sugars: sugars and sirups put in foods during preparation or processing, or at the table. ...
... This leads to rapid intracellular ATP depletion that stimulates AMP deaminase (AMPD) to catalyze the degradation of AMP to inosine monophosphate (IMP) leading to uric acid accumulation and Reactive Oxygen Species (ROS) within hepatic cells. The increase in intracellular uric acid is followed by an acute rise in uric acid in the circulation likely due to its release from the liver (Johnson, Perez-Pozo, et al. 2009;Johnson et al. 2013). ...
Fructose consumption in pediatric subjects is rising, as the prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH). Despite increasing evidence supporting the detrimental effects of fructose in the development of Metabolic Syndrome (MetS) and its related comorbidities, the association between fructose intake and liver disease remains unclear, mainly in youths. The current narrative review aims to illustrate the correlation between fructose metabolism and liver functions besides its impact on obesity and MASLD in pediatrics. Fructose metabolism is involved in the liver through the classical lipogenic pathway via de novo lipogenesis (DNL) or in the alternative pathway via uric acid accumulation. Hyperuricemia is one of the main features of MALSD patients, underlining how uric acid is growing interest as a new marker of disease. Observational and interventional studies conducted in children and adolescents, who consumed large amounts of fructose and glucose in their diet, were included. Most of these studies emphasized the association between high fructose intake and weight gain, dyslipidemia, insulin resistance, and MASLD/MASH, even in normal-weight children. Conversely, reducing fructose intake ameliorates liver fat accumulation, lipid profile, and weight. In conclusion, fructose seems a potent inducer of both insulin resistance and hepatic fat accumulation.
... Sucrose, the chemical component of sugar, is a disaccharide composed of glucose and fructose. Unlike glucose, fructose can act as a precursor for intracellular uric acid production, potentially increasing serum uric acid levels [8]. Recent epidemiologic studies in Western populations have shown a significant association between sugar-sweetened beverages (SSBs) and elevated serum uric acid levels [9][10][11][12][13][14][15], and excessive fructose consumption has also been shown to increase the risk of hyperuricemia and gout [9,15,16]. ...
Elevated uric acid levels are linked with obesity and diabetes. Existing research mainly examines the relationship between sugar-sweetened carbonated beverage (SSB) consumption and uric acid levels. This study explored the association between the quantity and frequency of SSB consumption and elevated uric acid levels in Korean adults. Data from 2881 participants aged 19–64 years (1066 men and 1815 women) in the 2016 Korea National Health and Nutrition Examination Survey were analyzed. Serum uric acid levels were categorized into quartiles, with the highest defined as high uric acid (men, ≥6.7 mg/dL; women, ≥4.8 mg/dL). SSB consumption was classified into quartiles (almost never, <1 cup (<200 mL), 1–3 cups (200–600 mL), ≥3 cups (≥600 mL)) and frequency into tertiles (almost never, ≤1/week, ≥2/week). Multivariate logistic regression assessed the association, with separate analyses for men and women. Increased daily SSB consumption and frequency were significantly associated with high uric acid levels in men but not in women. After adjusting for sociodemographic and health characteristics, consuming ≥3 cups (≥600 mL) of SSBs per day and SSBs ≥ 2/week were significantly associated with high serum uric acid levels in men, but this association was not observed in women. The study concludes that increased SSB intake is linked to elevated uric acid levels in Korean men, but not in women.
... Fructose metabolism diverges markedly from that of glucose, with unique implications for metabolic health. Unlike glucose, which is primarily metabolized in the liver, fructose metabolism occurs predominantly in the small intestine, leading to distinct metabolic outcomes that end up being transported to the liver via the portal vein (6). Excessive fructose intake can overwhelm hepatic metabolic pathways, resulting in the accumulation of metabolic intermediates and the deregulation of lipid metabolism, hence the dyslipidaemia and increase in free fatty acids associated with a high fructose diet (7). ...
Background: Modern diets high in fructose, have been linked to metabolic disorders, inflammation and oxidative stress. Herbal supplements like Cellgevity®, touted for their anti-inflammatory and antioxidant properties, therefore needed to be investigated. Objectives: This study was aimed to evaluate the potential of Cellgevity®, a herbal supplement, in preventing inflammation and oxidative stress, induced by a high fructose diet. Methods: Twenty male rats, (about 200g each), were divided into four groups of five rats each: the control, high fructose diet with fructose water (HFD+FW), HFD+FW with Atorvastatin (0.57 mg/kg-b.w), and HFD+FW with Cellgevity® (26.15 mg/kg-b.w), groups. After a 28-day experimental period, they were sacrificed and blood samples collected and analyzed for the levels of high sensitive C-reactive protein (HsCRP), malondialdehyde (MDA), and total antioxidant capacity (TAC). Statistical analysis, was done using the SPSS-20 package. Results: Rats on high fructose diet had significantly (P<0.05) elevated HsCRP levels (0.63±0.04 mg/dl) compared to those of the control (0.27±0.01 mg/dl). When compared with the HFD+FW group (0.63±0.04 mg/dl), Atorvastatin and Cellgevity® prevented significantly (P<0.05), the rise in HsCRP levels (0.28±0.00 mg/dl; 0.29±0.01 mg/dl respectively), while only Cellgevity® significantly (P<0.05) prevented an increase in the MDA levels (HFD+FW: 0.32±0.01 μM; Cellgevity®: 0.09±0.02 μM). Atorvastatin and Cellgevity® both significantly (P<0.05) prevented a fall in the TAC levels (0.38±0.03 μmol/ml; 0.59±0.03 μmol/ml respectively) compared to the HFD+FW group (0.21±0.06 μmol/ml), with Cellgevity® being more effective. Conclusion: Cellgevity® therefore showed promise as a supplement that can prevent high fructose diet induced inflammation and oxidative stress.
... 1 By 2025, the number of people living with hypertension is expected to reach 1.56 billion people. 2 Dietary factors that increase blood pressure (BP) are of interest to public health authorities. 3,4 The introduction of refined sugars into the food supply and the subsequent rise in sugar consumption has mirrored the increase in the prevalence of hypertension over the last century. 3 Sucrose is the most frequently used, and admired component to obtain sweetness in human food preparation. ...
Hypertension accounts for 10% of the total annual health budget in developed countries.1 By 2025, the number of people living with hypertension is expected to reach 1.56 billion people.2Dietary factors that increase blood pressure (BP) are of interest to public health authorities.3,4Twenty adult male Sprague-Dawley rats were taken. All groups received standard chow ad libitum. Controls (A), received plain drinking water, and the Sucrose treatment rats received 10% sucrose solution prepared daily for 12 weeks. Non-invasive blood pressure was recorded using computer based data recording system power lab model: M-ML 856, Australia with rat tail cuff attachment.Blood samples were collected. Serum aliquots were frozen at ?80°C for: ALT, AST, TG, total cholesterol (TC), and high-density lipoprotein (HDL) were determined using commercial enzymatic methods (CELM diagnosis, São Paulo, Brazil). The concentration of VLDL and low-density lipoprotein was measured. ANOVA and Post-Hoc Tukey tests were applied to determine statistical difference among the study groups. The results showed variable effects on biochemical and histopathological findings in rat liver, kidney and pancreas. The pancreas and kidneys of the rats showed adverse inflammatory histopathological changes maximally in rats taking jaggery syrup (Shakkar) flowed by white sugar and minimal in Shakkar. The adverse effects on liver cells were maximally seen on rats given brown sugar. This study enabled us to better understand the biochemical and histopathological effects of various types of sugars available in Pakistani market in order to create awareness regarding their effects on health.
... The intake of sugars such as high fructose corn syrup has increased significantly in the last decades, resulting in a dramatic increase in obesity, fatty liver, metabolic syndrome, and diabetes [36][37][38]. Several studies have also shown that a fructose-rich diet can raise uric acid production and induce components of the metabolic syndrome through mechanisms independent of energy intake or weight gain [39]. ...
Purpose of the Review
Our review explores the epidemiology, physiology, and clinical data surrounding the connection between hyperuricemia and metabolic syndrome, chronic kidney disease, and hypertension.
Recent Findings
Compelling physiologic mechanisms have been proposed to explain a causal relationship between hyperuricemia and metabolic syndrome, chronic kidney disease, and hypertension but clinical studies have given mixed results in terms of whether intervening with hyperuricemia using urate-lowering therapy has any beneficial effects for patients with these conditions.
Summary
Despite the large amount of research already put into this topic, more randomized placebo-controlled trials are needed to more firmly establish whether a cause-effect relationship exists and whether lowering uric acid levels in patients with these conditions is beneficial.
... With fruits as the primary fructose source until the latter half of the 20th century, the incorporation of HFCS into the Western diet marked a significant dietary alteration. This transition mirrors the unsettling rise in obesity and type 2 diabetes rates (Johnson, 2009). While HFCS itself is not inherently more obesogenic than other sugars, its ubiquity in processed foods and the subsequent ease of overconsumption spotlight it as a contributor to the obesity epidemic (Douard, 2018). ...
