scholarly journals Excessive fructose intake induces the features of metabolic syndrome in healthy adult men: role of uric acid in the hypertensive response

2009 ◽  
Vol 34 (3) ◽  
pp. 454-461 ◽  
Author(s):  
S E Perez-Pozo ◽  
J Schold ◽  
T Nakagawa ◽  
L G Sánchez-Lozada ◽  
R J Johnson ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Uric Acid ◽  
Healthy Adult ◽  
Adult Men ◽  
Fructose Intake

The causal role of elevated uric acid and waist circumference on the risk of metabolic syndrome components

2019 ◽  
Vol 44 (4) ◽  
pp. 865-874 ◽  
Author(s):  
Mahantesh I. Biradar ◽  
Kuang-Mao Chiang ◽  
Hsin-Chou Yang ◽  
Yen-Tsung Huang ◽  
Wen-Harn Pan
Keyword(s):  
Metabolic Syndrome ◽  
Uric Acid ◽  
Waist Circumference ◽  
Causal Role ◽  
Metabolic Syndrome Components

scholarly journals Review of Hyperuricemia as New Marker for Metabolic Syndrome

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Laura Billiet ◽  
Sarah Doaty ◽  
James D. Katz ◽  
Manuel T. Velasquez
Keyword(s):  
Metabolic Syndrome ◽  
Uric Acid ◽  
Lupus Erythematosus ◽  
Large Body ◽  
Epidemiologic Studies ◽  
Etiologic Factor ◽  
Systemic Diseases ◽  
Systemic Lupus ◽  
The Metabolic Syndrome

Hyperuricemia has long been established as the major etiologic factor in gout. In recent years, a large body of evidence has accumulated that suggests that hyperuricemia may play a role in the development and pathogenesis of a number of metabolic, hemodynamic, and systemic pathologic diseases, including metabolic syndrome, hypertension, stroke, and atherosclerosis. A number of epidemiologic studies have linked hyperuricemia with each of these disorders. In some studies, therapies that lower uric acid may prevent or improve certain components of the metabolic syndrome. There is an association between uric acid and the development of systemic lupus erythematosus; the connection between other rheumatic diseases such as rheumatoid arthritis and osteoarthritis is less clear. The mechanism for the role of uric acid in disorders other than gout is not well established but recent investigations point towards systemic inflammation induced by urate, as the major pathophysiological event common to systemic diseases, including atherosclerosis.

A possible role of serum uric acid as a marker of metabolic syndrome

2014 ◽  
Vol 44 (12a) ◽  
pp. 1210-1216 ◽  
Author(s):  
Y.-J. Lee ◽  
S. Cho ◽  
S. R. Kim
Keyword(s):  
Metabolic Syndrome ◽  
Uric Acid ◽  
Serum Uric Acid

scholarly journals Pregnancy Is Enough to Provoke Deleterious Effects in Descendants of Fructose-Fed Mothers and Their Fetuses

Nutrients ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 3667
Author(s):  
Elena Fauste ◽  
María I. Panadero ◽  
Cristina Donis ◽  
Paola Otero ◽  
Carlos Bocos
Keyword(s):  
Metabolic Syndrome ◽  
Lipid Peroxidation ◽  
Lipid Accumulation ◽  
Physiological State ◽  
Hormone Response ◽  
Female Progeny ◽  
Pregnant Rats ◽  
Fructose Intake ◽  
Hepatic Lipid Peroxidation

The role of fructose in the global obesity and metabolic syndrome epidemic is widely recognized. However, its consumption is allowed during pregnancy. We have previously demonstrated that maternal fructose intake in rats induces detrimental effects in fetuses. However, these effects only appeared in adult descendants after a re-exposure to fructose. Pregnancy is a physiological state that leads to profound changes in metabolism and hormone response. Therefore, we wanted to establish if pregnancy in the progeny of fructose-fed mothers was also able to provoke an unhealthy situation. Pregnant rats from fructose-fed mothers (10% w/v) subjected (FF) or not (FC) to a fructose supplementation were studied and compared to pregnant control rats (CC). An OGTT was performed on the 20th day of gestation, and they were sacrificed on the 21st day. Plasma and tissues from mothers and fetuses were analyzed. Although FF mothers showed higher AUC insulin values after OGTT in comparison to FC and CC rats, ISI was lower and leptinemia was higher in FC and FF rats than in the CC group. Accordingly, lipid accretion was observed both in liver and placenta in the FC and FF groups. Interestingly, fetuses from FC and FF mothers also showed the same profile observed in their mothers on lipid accumulation, leptinemia, and ISI. Moreover, hepatic lipid peroxidation was even more augmented in fetuses from FC dams than those of FF mothers. Maternal fructose intake produces in female progeny changes that alter their own pregnancy, leading to deleterious effects in their fetuses.

scholarly journals Brief Report:  An Evolutionary Basis to Cancer Growth

2021 ◽  
Author(s):  
Mehdi Fini ◽  
Eric Gaucher ◽  
Brian Boutwell ◽  
Takahiko Nakagawa ◽  
Richard Wright ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Uric Acid ◽  
Tumor Growth ◽  
Meta Analysis ◽  
Survival Advantage ◽  
Thrifty Gene ◽  
Added Sugars ◽  
Fructose Intake ◽  
Increased Risk ◽  
Excessive Intake

Abstract Background. Recently we have reviewed the evidence that excessive intake of fructose, present in added sugars, may be a unique nutrient that stimulates tumor growth while also causing obesity and metabolic syndrome, thereby providing one of the reasons why obesity is associated with increased risk for various cancers. Prior studies have suggested that one of the reasons fructose increases the risk for cancer may be due in part to its metabolite uric acid, and both a meta-analysis and Mendelian randomization study confirm uric acid is a risk factor. Here we suggest that a mutation in uric acid metabolism may have provided survival advantage to our ancestors but ironically increase our risk for cancer today.Methods. Ancestral humans lost the gene uricase during the mid-Miocene where it led to higher uric acid levels that facilitated the effects of fructose to stimulate fat accumulation. Here we tested whether a loss of uricase would also facilitate tumor growth. Experiments were performed in mice in which uricase was inactivated by either knocking out the gene or by inhibiting uricase with oxonic acid. We also studied mice transgenic for uricase. These mice were injected with breast cancer cells and followed for 4 weeks.Results. The inhibition or knockout of uricase was associated with a remarkable increase in tumor growth and metastases. In contrast, transgenic uricase mice showed reduced tumor growth.Conclusion. A loss of uricase increases the risk for tumor growth. Prior studies have shown that the loss of the mutation facilitated the ability of fructose to increase fat which provided a survival advantage for our ancestors that came close to extinction from starvation in the mid Miocene. Today, however, excessive fructose intake is rampant and increasing our risk not only for obesity and metabolic syndrome, but also cancer. Obesity-associated cancer may be due, in part, to a mutation 15 million years ago that acted as a thrifty gene.

Abstract P231: Uric Acid Is Associated with Metabolic Syndrome in Children and Adults: The Bogalusa Heart Study

Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Dianjianyi Sun ◽  
Xiaotao Zhang ◽  
Shengxu Li ◽  
Camilo Fernandez ◽  
Wei Chen ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Uric Acid ◽  
Elevated Serum ◽  
Hdl Cholesterol ◽  
Model Assessment ◽  
Continuous Variables ◽  
Cholesterol Ratio ◽  
Heart Study ◽  
Age Trends

Background: Elevated serum uric acid (UA) is commonly found in subjects with metabolic syndrome (MetS). This study assessed the hypothesis that UA is associated with levels of individual MetS components and the degree of their clustering patterns in different age periods. Methods: The study sample consisted of 2614 children (1577 whites, 1037 blacks; 1333 males; aged 4-18 years) and 2447 adults (1682 whites, 1765 blacks; 1072 males; aged 19-54 years) examined during 1987-2010. The adverse levels of MetS components, including body mass index (BMI), mean arterial pressure (MAP), triglycerides to HDL cholesterol ratio (TG/HDLC), and homeostasis model assessment of insulin resistance (HOMA), were defined as >75th percentile specific for age, race and sex. Observed/expected (O/E) ratio and intra-class correlation (ICC) were used as a measure of the degree of clustering of categorical and continuous variables, respectively. Results: UA was significantly positively associated with only BMI in children, and with all four components in adults. Odds ratios of UA associated with MetS were 1.74 in children and 1.92 in adults (p<0.001 for both), adjusted for race, sex and age. Trends in O/E ratios with UA quartiles are shown in the figure below. ICCs of 3- and 4-component clusters increased with increasing UA quartiles in children; however, only BMI-MAP-HOMA cluster showed an increasing trend of ICC in adults. Conclusions: The results suggest an important role of UA in the development of MetS in pediatric and adult populations. The findings provide further insights into the potential pathophysiological mechanisms of MetS and have implications for identification and treatment of high risk individuals for MetS in early life.

A causal role for uric acid in fructose-induced metabolic syndrome

2006 ◽  
Vol 290 (3) ◽  
pp. F625-F631 ◽  
Author(s):  
Takahiko Nakagawa ◽  
Hanbo Hu ◽  
Sergey Zharikov ◽  
Katherine R. Tuttle ◽  
Robert A. Short ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Metabolic Syndrome ◽  
Uric Acid ◽  
Endothelial Function ◽  
Control Diet ◽  
Oxidase Inhibitor ◽  
Xanthine Oxidase Inhibitor ◽  
Fructose Intake ◽  
High Fructose ◽  
Aortic Artery

The worldwide epidemic of metabolic syndrome correlates with an elevation in serum uric acid as well as a marked increase in total fructose intake (in the form of table sugar and high-fructose corn syrup). Fructose raises uric acid, and the latter inhibits nitric oxide bioavailability. Because insulin requires nitric oxide to stimulate glucose uptake, we hypothesized that fructose-induced hyperuricemia may have a pathogenic role in metabolic syndrome. Four sets of experiments were performed. First, pair-feeding studies showed that fructose, and not dextrose, induced features (hyperinsulinemia, hypertriglyceridemia, and hyperuricemia) of metabolic syndrome. Second, in rats receiving a high-fructose diet, the lowering of uric acid with either allopurinol (a xanthine oxidase inhibitor) or benzbromarone (a uricosuric agent) was able to prevent or reverse features of metabolic syndrome. In particular, the administration of allopurinol prophylactically prevented fructose-induced hyperinsulinemia (272.3 vs.160.8 pmol/l, P < 0.05), systolic hypertension (142 vs. 133 mmHg, P < 0.05), hypertriglyceridemia (233.7 vs. 65.4 mg/dl, P < 0.01), and weight gain (455 vs. 425 g, P < 0.05) at 8 wk. Neither allopurinol nor benzbromarone affected dietary intake of control diet in rats. Finally, uric acid dose dependently inhibited endothelial function as manifested by a reduced vasodilatory response of aortic artery rings to acetylcholine. These data provide the first evidence that uric acid may be a cause of metabolic syndrome, possibly due to its ability to inhibit endothelial function. Fructose may have a major role in the epidemic of metabolic syndrome and obesity due to its ability to raise uric acid.

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