Fructose overconsumption leads to dyslipidaemia and ectopic lipid deposition
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Nonalcoholic fatty liver disease and insulin resistance have been accounted for by both nutritional and genetic factors. Depending on metabolic status, liver metabolism of dietary fructose will activate either gluconeogenesis/glycogen synthesis or lipogenesis. The study aimed to assess the effects of fructose, a potent stimulator of hepatic de novo lipogenesis, on intrahepatocellular lipids (IHCLs) and insulin sensitivity in healthy offspring of patients with type 2 diabetes (OffT2D), who are prone to metabolic disorders related to insulin resistance. By means of a cross-over design, 16 male OffT2D and 8 control subjects were studied after either a 7-day isocaloric diet or a hypercaloric high-fructose diet, hepatic and whole-body insulin sensitivity being assessed with a 2-step hyperinsulinaemic euglycaemic clamp. IHCLs and intramyocellular lipids (IMCLs) were measured by proton magnetic resonance spectroscopy. Compared with the control group, the OffT2D group exhibited significantly higher IHCLs, total triglycerides, and lower whole-body insulin sensitivity. The high-fructose diet was associated with a significant increase in IHCLs, IMCLs, VDLD-triglycerides, and fasting hepatic glucose output. Moreover, the effects of fructose on VLDL-triglycerides were significantly higher in the OffT2D group. These results suggest that these subjects might be more prone to developing atherogenic dyslipidaemia when challenged by high-fructose intake.
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