Acute, food-induced moderate elevation of plasma uric acid protects against hyperoxia-induced oxidative stress and increase in arterial stiffness in healthy humans

Vuković, Jonatan; Modun, Darko; Budimir, Danijela; Sutlović, Davorka; Salamunić, Ilza; Žaja, Ivan; Boban, Mladen

doi:10.1016/j.atherosclerosis.2009.04.012

Cited by 35 publications

(26 citation statements)

References 54 publications

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“…24,25 Transient postprandial increases in uric acid have been associated with reducing hyperoxia-induced oxidative stress and mitigated consequential rises in arterial stiffness. 26 Our finding of a small decrease in uric acid concentration following glucose ingestion is curious, although it is an effect that has been found in a longer-term setting. Over a 2-week period during which participants consumed either a fructose-or glucoseenriched diet in a randomised crossover design, fasting uric acid concentration tended to decrease relative to baseline and was lower during the glucose compared with the fructose period.…”

Section: Discussionmentioning

confidence: 77%

Acute effect of fructose intake from sugar-sweetened beverages on plasma uric acid: a randomised controlled trial

et al. 2016

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Section: Discussionmentioning

confidence: 77%

Acute effect of fructose intake from sugar-sweetened beverages on plasma uric acid: a randomised controlled trial

et al. 2016

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“…However, recent observations also suggest that food-induced moderate elevation of uric acid can protect against arterial stiffening in healthy humans. Indeed, consumption of fructose was shown to prevent the increase in hypoxia-induced arterial stiffness [68], an effect partially explained by an increase in plasma uric acid concentrations. In the present study, we used CJC and PJ containing similar quantities of fructose and no significant variation in circulating uric acid concentrations following either CJC or PJ.…”

Section: Discussionmentioning

confidence: 99%

Evidence that cranberry juice may improve augmentation index in overweight men

et al. 2013

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“…Ethanol consumption is implicated as a cause of hyperuricemia (13,14,24,43), and combined administration of ethanol (0.7 mol) and glycerol (0.02 mol) caused a similar elevation of serum uric acid in humans as fructose (0.4 mol) (38). We tested the separate effects of glycerol and ethanol (Fig.…”

Section: Uap From Endogenous Substrates In Hepatocytesmentioning

confidence: 99%

“…Intravenous fructose infusion at concentrations Ͼ5 mM lowers hepatic P i and ATP in humans and rats (21) and raises blood uric acid in humans (15,23,38), but whether dietary fructose elicits effects on UAP is uncertain because fructose levels in the portal vein after oral ingestion are thought not to exceed 2.5 mM (16,34). We next tested the effect of fructose (2-20 mM) at either basal (5 mM) or elevated (15-25 mM) glucose to simulate glucose concentrations in the portal vein after carbohydrate-containing meals.…”

Section: Uap From Endogenous Substrates In Hepatocytesmentioning

confidence: 99%

The rate of production of uric acid by hepatocytes is a sensitive index of compromised cell ATP homeostasis

Petrie

Patman

Sinha

et al. 2013

American Journal of Physiology-Endocrinology and Metabolism

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Petrie JL, Patman GL, Sinha I, Alexander TD, Reeves HL, Agius L. The rate of production of uric acid by hepatocytes is a sensitive index of compromised cell ATP homeostasis. Am J Physiol Endocrinol Metab 305: E1255-E1265, 2013. First published September 17, 2013; doi:10.1152/ajpendo.00214.2013.-Plasma levels of uric acid, the final product of purine degradation in humans, are elevated in metabolic syndrome and are strongly associated with insulin resistance and nonalcoholic fatty liver disease (NAFLD). Hepatic and blood levels of purine metabolites (inosine, hypoxanthine, and xanthine) are also altered in pathophysiological states. We optimized a rat hepatocyte model to test the hypothesis that the production of uric acid by hepatocytes is a potential marker of compromised homeostasis of hepatocellular inorganic phosphate (Pi) and/or ATP. The basal rate of uric acid production from endogenous substrates in rat hepatocytes was comparable to that in human liver and was Ͻ10% of the maximum rate with saturating concentrations of purine substrates. It was marginally (ϳ20%) decreased by insulin and increased by glucagon but was stimulated more than twofold by substrates (fructose and glycerol) that lower both cell ATP and Pi, and by inhibitors of mitochondrial respiration (complexes I, III, and V) that lower ATP but raise cell Pi. Clearance of inosine and its degradation to uric acid were also inhibited by cell Pi depletion. Analysis of gene expression in NAFLD biopsies showed an association between mRNA expression of GCKR, the glucokinase regulatory protein that is functionally linked to uric acid production, and mRNA expression of the phosphate transporters encoded by SLC17A1/3. Uric acid production by hepatocytes is a very sensitive index of ATP depletion irrespective of whether cell Pi is lowered or raised. This suggests that raised plasma uric acid may be a marker of compromised hepatic ATP homeostasis. nonalcoholic fatty liver disease; hyperuricemia; fructose; mitochondrial function PLASMA LEVELS OF URIC ACID, the final product of purine degradation in humans (Fig. 1), are strongly associated with insulin resistance (39) and with nonalcoholic fatty liver disease (NAFLD) (2,20,28). Plasma uric acid reflects the balance between endogenous production by the liver and excretion by the kidney and gut (29). Genome meta-analyses identified common variants in the GCKR gene, which encodes the inhibitor protein of liver glucokinase (GCK) in association with raised serum uric acid levels (18,19,44), and functional studies confirmed a link between GCKR expression in hepatocytes and uric acid production (UAP) (3, 5). However, the minor GCKR variant that associates with raised uric acid levels and hepatic steatosis is associated with decreased rather than increased insulin resistance (26, 31). This indicates that other factors must contribute to the association of hyperuricemia and insulin resistance (39).Lifestyle factors linked to hyperuricemia include obesity and consumption of fructose or ethanol (1, 39, 43). Of these, fr...

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Acute, food-induced moderate elevation of plasma uric acid protects against hyperoxia-induced oxidative stress and increase in arterial stiffness in healthy humans

Cited by 35 publications

References 54 publications

Acute effect of fructose intake from sugar-sweetened beverages on plasma uric acid: a randomised controlled trial

Acute effect of fructose intake from sugar-sweetened beverages on plasma uric acid: a randomised controlled trial

Evidence that cranberry juice may improve augmentation index in overweight men

The rate of production of uric acid by hepatocytes is a sensitive index of compromised cell ATP homeostasis

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