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A causal role for uric acid in fructose-induced metabolic syndrome.
TLDR
The first evidence that uric acid may be a cause of metabolic syndrome is provided, possibly due to its ability to inhibit endothelial function, as well as a reduced vasodilatory response of aortic artery rings to acetylcholine. Expand
A role for uric acid in the progression of renal disease.
TLDR
Hyperuricemia accelerates renal progression in the RK model via a mechanism linked to high systemic BP and COX-2-mediated, thromboxane-induced vascular disease and provides direct evidence that uric acid may be a true mediator of renal disease and progression. Expand
Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease.
TLDR
It is suggested that high intakes of fructose in African Americans may explain their greater predisposition to develop cardiorenal disease, and a list of testable predictions to evaluate this hypothesis is provided. Expand
Hyperuricemia induces a primary renal arteriolopathy in rats by a blood pressure-independent mechanism.
TLDR
Hyperuricemia induces a renal arteriolopathy in rats that is blood pressure independent and involves the renin-angiotensin system, and this was partially inhibited by losartan. Expand
Hyperuricemia induces endothelial dysfunction.
TLDR
Uric acid was found to inhibit both basal and vascular endothelial growth factor (VEGF)-induced nitric oxide production in bovine aortic endothelial cells and may provide insight into a pathogenic mechanism by which uric acid may induce hypertension and vascular disease. Expand
Sugar, Uric Acid, and the Etiology of Diabetes and Obesity
TLDR
The hypothesis that fructose-mediated generation of uric acid may have a causal role in diabetes and obesity is revisited and new insights into pathogenesis and therapies for this important disease are provided. Expand
Uric Acid Induces Hepatic Steatosis by Generation of Mitochondrial Oxidative Stress
TLDR
It is shown that fructose also stimulates triglyceride synthesis via a purine-degrading pathway that is triggered from the rapid phosphorylation of fructose by fructokinase, which provides new insights into the pathogenesis of hepatic fat accumulation under normal and diseased states. Expand
Adverse effects of the classic antioxidant uric acid in adipocytes: NADPH oxidase-mediated oxidative/nitrosative stress.
TLDR
It is demonstrated that differentiation of cultured mouse adipocytes is associated with increased production of reactive oxygen species (ROS) and uptake of uric acid and hyperuricemia-induced alterations in oxidative homeostasis in the adipose tissue might play an important role in these derangements. Expand
Fructose-induced metabolic syndrome is associated with glomerular hypertension and renal microvascular damage in rats.
TLDR
Fructose-induced metabolic syndrome is associated with renal disturbances characterized by renal hypertrophy, arteriolopathy, glomerular hypertension, and cortical vasoconstriction, best observed in rats administered high doses (60% diet) of fructose. Expand
Hypothesis: could excessive fructose intake and uric acid cause type 2 diabetes?
TLDR
It is proposed that excessive fructose intake (>50 g/d) may be one of the underlying etiologies of metabolic syndrome and type 2 diabetes and simple public health measures could have a major impact on improving the overall health of the populace. Expand
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