Dietary fructose and metabolic dysregulation

Abstract

Human dietary fructose consumption has increased substantially over the last century, as has the incidence of obesity and insulin resistance syndromes. This review concerns metabolic dysregulation resulting from high fructose consumption. Fructose metabolism is largely unregulated and results in rapid depletion of ATP and a consequent increase in the level of uric acid (hyperuricemia). In most animals, uric acid is converted to allantoin by uricase and is excreted. However, in primates, which lack uricase, hyperuricemia induced by excessive fructose consumption results in a wide range of symptoms, including obesity, insulin resistance, type II diabetes mellitus, hypertriglyceridemia, fatty liver disease, functional bowel disturbances and hypertension, collectively termed metabolic syndrome. The search for suitable animal models to study these phenomena is being actively pursued at present.