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

By T. Nakagawa, Hanbo Hu, Sergey I Zharikov, Katherine R. Tuttle, R. Short, Olena Y. Glushakova, Xiaosen Ouyang, D. Feig, E. Block, J. Herrera-Acosta and 2 more. AJP - Renal Physiology, 2006

1,149 citations recorded by the source corpus.

Subfields: Endocrinology, Diabetes and Metabolism, Epidemiology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/02ceda4f7736432d58729c8e0fe82d8f3b8bf163

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Endocrinology, Diabetes and Metabolism

1. Richard J. Johnson
2. F. B. Hu
3. K. Stanhope

In Epidemiology

1. T. Nakagawa
2. Richard J. Johnson
3. A. Diehl
4. Sergey I Zharikov
5. Y. Sautin
6. F. B. Hu
7. K. Stanhope

In Pathology and Forensic Medicine

1. F. B. Hu
2. K. Stanhope

Citations in the corpus

• Uric Acid Induces Hepatic Steatosis by Generation of Mitochondrial Oxidative Stress (2012, background): “In this context, our group and others have reported that lowering uric acid can block both fructose-induced metabolic syndrome as well as improve features of metabolic syndrome in other animal models (32, 46).”
• Pro v Con Debate: Role of sugar sweetened beverages in obesity Resolved: there is sufficient scientific evidence that decreasing sugar-sweetened beverage consumption will reduce the prevalence of obesity and obesity-related diseases (2013, neutral): “In the Nurses’ Health Study, we found that regular SSB intake was significantly associated with increased incidence of CHD (non-fatal myocardial infarction or fatal CHD) (46).”
• Adverse effects of the classic antioxidant uric acid in adipocytes: NADPH oxidase-mediated oxidative/nitrosative stress. (2007, background): “Most importantly, it has been shown recently that uric acid has a causal role in the metabolic syndrome induced by fructose (41).”
• Fructose and Sugar: A Major Mediator of Nonalcoholic Fatty Liver Disease (2018, neutral): “68 j 10 between groups.(37,40) Indeed, one can even induce fatty liver with a calorically restricted diet if the diet is high (40%) in sugar.”
• Fructose consumption as a risk factor for non-alcoholic fatty liver disease. (2008, background): “There is also increasing evidence that the rise in uric acid may also have a potential role in causing features of the metabolic syndrome [18], in part by the ability of uric acid to deplete endothelial nitric oxide levels [45] and by activating the adipocyte [32].”
• Sugar, Uric Acid, and the Etiology of Diabetes and Obesity (2013, background): “For example, rats fed fructose develop fatty liver, hypertriglyceridemia, and insulin resistance when compared with rats fed isocaloric glucose or starch-enriched diets (4,5).”
• Role of Dietary Fructose and Hepatic de novo Lipogenesis in Fatty Liver Disease (2016, background): “DNL requires ATP in order to synthesize lipids from dietary carbohydrates, while rapid phosphorylation of fructose to fructose-1 phosphate depletes hepatic ATP levels and leads to uric acid production [108].”
• Uric acid and chronic kidney disease: which is chasing which? (2013, background): “The administration of fructose to rats also reproduces most of the renal hemodynamic effects of experimental hyperuricemia and can also cause renal disease that can be blocked by lowering uric acid levels [51, 52].”
• Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease. (2007, background): “As in humans, it was shown that the active ingredient is fructose rather than glucose: feeding fructose to rats resulted in the metabolic syndrome, whereas equivalent amounts of glucose or starch did not induce these features (51).”
• INCREASED FRUCTOSE CONSUMPTION IS ASSOCIATED WITH FIBROSIS SEVERITY IN PATIENTS WITH NAFLD (2010, background): “In experimental animals, lowering uric acid concentrations ameliorated features of the metabolic syndrome induced by fructose, including weight gain, hypertriglyceridemia, hyperinsulinemia and insulin resistance, and hypertension.(34) These findings were surprising, because most authorities had cons”