Excessive fructose consumption is associated with the development of metabolic syndrome and type II diabetes. Both conditions are well-known risk factors for cardiovascular and renal diseases. Uric acid synthesis is linked biochemically to fructose metabolism, thus the widespread consumption of this monosaccharide has been related to steady increasing levels of serum uric acid during the past few decades. Recent evidence has suggested that uric acid may act as a cardiorenal toxin. In this regard, experimental studies have suggested that the primary noxious effect of uric acid occurs inside the cell and is likely the stimulation of oxidative stress. More studies to disclose the harmful mechanisms associated with increasing intracellular uric acid levels after a fructose load are warranted.
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