Fructose-Induced Hyperuricemia Is Associated With a Decreased Renal Uric Acid Excretion in Humans. Virgile Lecoultre, PHD1,; Léonie Egli, MSC1,; Fanny. Fructose-induced hyperuricemia and hyperuricaciduria is associated with a striking increase in the blood lactate concentration, a decrease in erythrocyte. As such, we propose that the epidemic of the metabolic syndrome is due in part to fructose-induced hyperuricemia that reduces endothelial NO levels and.

Author: Fenrikazahn Zulunris
Country: Turkey
Language: English (Spanish)
Genre: Art
Published (Last): 1 March 2014
Pages: 192
PDF File Size: 9.36 Mb
ePub File Size: 18.39 Mb
ISBN: 524-3-54680-252-1
Downloads: 75378
Price: Free* [*Free Regsitration Required]
Uploader: Digar

Parts of this study were presented in abstract form at Experimental BiologyBoston, Massachusetts, 20—24 April These studies support the hypothesis that fructose-induced hyperuricemia results from degradation of adenosine monophosphate. As such, we propose that the epidemic of the metabolic syndrome is due in part to fructose-induced hyperuricemia that reduces endothelial NO levels and induces insulin resistance. Fructose-induced hyperuricemia results in endothelial dysfunction and insulin resistance, and might be a novel causal mechanism of the metabolic syndrome.

This effect appears to be specific for fructose. Open in a separate window. Nutr Metab Lond ; 9: After the infusion of fructose, 0. In three patients with galactosemia, increases in blood uric acid levels after galactose ingestion were similar to those in normal children after fructose, but less than those in patients with HFI after fructose. Support Center Support Center.

This study was supported by grant from the Swiss National Foundation for Science and by a grant from Ajinomoto Co. Hyperurocemia in humans should be performed to address whether lowering uric acid levels will help to prevent this condition. Journal List Diabetes Care v. Furthermore, high-fructose intake over several days is associated with increased fasting UA concentration 1.

Am J Physiol Renal Physiol ; The serum Pi levels decreased less in galactosemic patients after galactose administration than in patients with HFI after fructose infusion.

  HUGO CHAVEZ AND THE BOLIVARIAN REVOLUTION RICHARD GOTT PDF

F—F [ PubMed ].

NO increases blood flow to skeletal muscle and enhances glucose uptake. Although the cumulative indduced load was large 1. Because the metabolic effects of fructose show significant sex differences, it remains to be assessed whether the same effects are observed in female subjects.

The serum Pi level decreased 2. It has not been assessed, however, whether UA also increases when fructose is administered as several small drinks instead of one single large load or fguctose a high-fructose diet HFrD impairs renal UA clearance UAC or fractional excretion UAFE as observed in rats 3.

Closed symbols represent data collected after 4—6 days of HFrD. The lack of hyperruricemia in galactosemia patients after galactose ingestion may be explained by the observation that galactose is phosphorylated more slowly than fructose.

Fructose-Induced Hyperuricemia Is Associated With a Decreased Renal Uric Acid Excretion in Humans

Fructose–unlike other sugars–causes serum uric acid levels to rise rapidly. Am J Clin Nutr ; Urinary UA excretion rate. Blood glucose, lactic acid, and fructose levels were significantly increased after fructose, but serum magnesium levels did not change.

Allopurinol, rutin, and quercetin attenuate hyperuricemia and renal dysfunction in rats induced by fructose intake: Published online Aug No other potential conflicts of interest relevant to this article were reported.

Acknowledgments This study was supported by grant from the Swiss National Foundation for Science and by a grant from Ajinomoto Co.

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. In two patients with HFI the uric acid excretion increased four- to fivefold after fructose administration; the increased uric acid excretion in HFI exceeded that of normal children.

Please review our privacy policy. Exercise prevents fructose-induced hypertriglyceridemia in healthy young subjects. The mean blood inorganic phosphate Pi levels were significantly less than the mean fasting value after fructose.

  BLOOMA WESTPOINT PDF

Animals deficient in endothelial NO develop insulin resistance and other features of the metabolic syndrome. Ingestion of a high-fructose meal increases blood uric acid UA concentration in healthy subjects 1.

Fructose-Induced Hyperuricemia Is Associated With a Decreased Renal Uric Acid Excretion in Humans

We recently reported that uric acid reduces levels of endothelial nitric oxide NOa key mediator of insulin action. National Center for Biotechnology InformationU.

This article has been cited by other articles in PMC. Effects of supplementation with essential amino acids on intrahepatic lipid concentrations during fructose overfeeding in humans. This mechanism may substantially enhance the risk of gout in people who consume high amounts of sugar. These effects are generally attributed to an increased UA production, as observed after intravenous fructose administration 2.

These samples were collected while subjects were participating in two clinical trials clinical trial reg. These observations suggest that a decreased urinary UA excretion may contribute to fructose-induced hyperuricemia.

In two patients with hereditary fructose intolerance HFI the peak blood uric acid levels were Consistent with this hypothesis is the observation that changes in mean uric acid levels correlate with the increasing prevalence of metabolic syndrome in the US and developing countries. The increasing incidence of obesity and the metabolic syndrome over the past two decades has coincided with a marked increase in total fructose intake.

The mean uric acid excretion, expressed as milligrams per mg urinary creatinine, was 0. In addition, we observed that a serum uric acid level above 5.

Author information Copyright and License information Disclaimer.