Fructose Intake, Serum Uric Acid, and Cardiometabolic Disorders: A Critical Review

On April 18, Caliceti et al. published a review entitled “Fructose Intake, Serum Uric Acid, and Cardiometabolic Disorders: A Critical Review” in Nutrients. The review focuses on the role of uric acid (UA) in cardio metabolic disorders and the relationship between fructose consumption, blood UA, and health outcomes.

The authors first review purine metabolism including purine generation via two pathways 1) purine salvage pathway and 2) de novo synthesis from non-purine compounds followed the catabolism of purines which is regulated by xanthine-oxidoreductase (XOR) which codes for the xanthine dehydrogenase (XDH) and xanthine oxidase (XO) enzymes. The mechanisms of XDH and XO result in UA production. Authors note that most UA is filtered through the kidneys and is excreted in the urine, the rest is metabolized by gut microbiota in the intestine and is eliminated in the feces. UA reabsorption and secretion have a number of mediators that help regulate UA concentrations.

Authors note that metabolism of fructose is known to stimulate UA production through purine degradation which generates mitochondrial oxidants. The mitochondrial oxidative stress results in stimulation of fatty acid synthase and therefore promotes de novo lipogenesis and hepatic fat accumulation. Authors also cite researcher suggesting that fructose stimulates UA synthesis from amino acid precursors such as glycine and that chronic fructose consumption can inhibit renal excretion of UA resulting increased serum UA, though this last point is not well supported.

Next, author’s present data which suggest that UA can act as an intracellular prooxidant under inflammatory conditions, as in the case of arterial plaque formation. UA has also been found to induce intracellular oxidative stress by stimulating NOX and altering mitochondrial function which can result in fat synthesis. Another oxidative stress hypothesis is that intracellular XO activity and increased reactive oxygen species (ROS) production can result in endothelial dysfunction and lead to hypertension.

Authors then detail in vivo literature pertaining to the topic which is largely contradictory and controversial due to the inability for population-based studies to adjust for confounding variables. The paper concludes “a specific causal link between fructose consumption, hyperuricemia, and CVS has not yet been established…it is not yet possible to conclude that fructose intake is the main contributor to an increase in blood UA, and that this detrimentally affects vascular health.”

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