Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans These data suggest that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults.

People suffering from the metabolic syndrome have higher baseline circulating FGF21 levels and exhibit a larger increase of plasma FGF21 concentrations following an oral fructose load. In contrast, the increase of FGF21 after ingestion of the same amount of glucose was delayed and much more modest. These results are paradoxical in that the metabolic effects of FGF-21 appear to be mainly beneficial while those of dietary fructose are generally deleterious [3]. The authors suggest the possibility that obese subjects with metabolic syndrome are resistant to the actions of FGF21 (akin to augmentation of circulating insulin and leptin concentrations and responses in insulin and leptin resistance) and that the exaggerated response to fructose ingestion may be a compensatory response [1]. The increases of FGF-21 in response to fructose ingestion across normal weight and overweight/obese subjects was significantly correlated with circulating insulin and glucose levels in response to oral glucose loads suggesting a relationship between FGF21 and insulin senstivity/glucose tolerance. Together, these novel results shed light on a potential mechanism related to the adverse metabolic effects of dietary fructose and raise new questions about the nutritional regulation of metabolic responses to dietary macronutrients, specifically sugars.

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