Metabolic syndrome is a condition characterised by metabolic dysfunction and insulin resistance. Evidence suggests that metabolic syndrome is implicated in the development of a large percentage of the obesity cases Worldwide. The metabolic changes associated with obesity are though to lead to systemic inflammation which may cause a depletion of cellular and extracellular antioxidant. This pro-inflammatory state is thought to increase the risk of developing diabetes and cardiovascular disease. Metabolic syndrome is thought to be caused by a combination of genetic and dietary factors. Fructose overconsumption has been strongly implicated in the development of the metabolic syndrome in a number of studies, because fructose can stimulate de novo lipogenesis in the liver. It is thought that the increase in fatty acids may contribute to insulin resistance and non-alcoholic fatty liver disease via the accumulation of intramyocellular and intrahepatocellular lipids, respectively.
Because there is a likely genetic component to the development of metabolic syndrome, offspring of parents with type 2 diabetes are prone to metabolic disorders. Therefore the effect of fructose consumption on insulin sensitivity, and the accumulation of intrahepatocellular and intramyocellular lipids has been investigated1 in individuals who have at least one parent with type 2 diabetes. Control subjects where selected who did not have either parent with type 2 diabetes. The subjects were randomly fed either an isocaloric diet for 7 days or a high fructose (3.5 grams per kg of fat free mass per day) high calorie (+35% energy intake) diet before being crossed over to the other treatment. Researcher measured hepatic and whole body insulin sensitivity with a 2-step hyperinsulinaemic euglycaemic clamp and 6,6-[2H2]glucose and intrahepatocellular lipids by 1H-magnetic resonance imaging.
At baseline the diabetes group had significantly higher intrahepatocellular lipids (+94%) and total tiacylglycerols (+35%) as well as lower whole body insulin sensitivity (-27%) compared to the control group. Following the high fructose diet there was an increase in intrahepatocellular lipids (+76% in the diabetes group, +79% in the control group); intramyocellular lipids (+47% in the diabetes group, +24% in the control group); very low density triacylglycerols (+110% in the diabetes group, +51% in the control group); and fasting hepatic glucose output (+4% in the diabetes group, +5% in the control group). These results show that high fructose consumption along with a hypercaloric diet causes increased lipid deposition in muscle and liver and decreases insulin sensitivity. The fructose treatment had a greater effect on de novo lipogenesis in the diabetes group, suggesting that individuals with a family history of diabetes may be more susceptible to fructose induced metabolic dysfunction.
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