Fructose at the crossroads of the metabolic syndrome and obesity epidemics.

In this review, we highlight the specific metabolic effects of fructose consumption that are involved in the development of metabolic syndrome non-alcoholic fatty liver disease and its association with obesity. The specifics effects of fructose on the liver are particularly germane to the development of a vicious cycle that starts with liver steatosis driving insulin resistance. These effects include 1) increased de novo lipogenesis, 2) increased liver fat, 3) dyslipidemia 4) increased uric acid production which feeds back on increased fructose metabolism and, 5) increased methylglyoxal and Maillard reaction that may affect adenosyl-monophosphate-dependent kinase Fructose increases cortisol activation especially in visceral fat. The hormones involved in satiety control are affected by fructose consumption. Fructose derived advance glycation end-products  may also induce a state of inflammation by engaging its receptor, RAGE. Directionality for the effect of fructose on metabolic syndrome is becoming clear: fructose drives hepatic fat, which in turn drives insulin resistance. There is an urgent need for more clinical and educational interventions to regulate/reduce fructose consumption in our population, especially in children and adolescents.