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Although the pathogenesis of nonalcoholic fatty liver disease (NAFLD) is complex, increasing evidence suggests that fructose is a contributing factor. In the search for dietary triggers for NAFLD, fructose has been consistently identified as a candidate; this makes sense, given the metabolic events attendant to fructose ingestion. The digestion, absorption, and metabolism of fructose differ from those of glucose.[1] Unlike glucose, fructose does not stimulate insulin secretion, enhance leptin production, or suppress hunger. Insulin and leptin are key afferent signals in the regulation of food intake and body weight; thus, dietary fructose may contribute to increased energy intake and weight gain. Hepatic metabolism of fructose has been shown to elicit potentially deleterious metabolic perturbations -- risk factors for NAFLD. Consumption of fructose-sweetened but not glucose-sweetened beverages increases fat mass, visceral adiposity, de novo lipogenesis, and inflammation, and it induces insulin resistance and postprandial hypertriglyceridemia, particularly in overweight individuals.[