Fructose is thought to be the cause of the obesity epidemic currently engulfing Western nations. Traditionally, the human diet has contained carbohydrates in their unrefined forms. Although processed through milling, the final grains product still retained the original constituents of the plant material, including the germ, endosperm and bran. However, modern refining processes have allowed removal of the bran and germ layers, leaving only the starchy endosperm. This increases digestion speed considerably and increasing intakes of such refined carbohydrates may contribute to insulin resistance and obesity. However, it is likely that in order to cause excessive adiposity seen in obese individuals, another agent is required in addition to the consumption of refined carbohydrates. Evidence suggests that the molecule fructose may be partly responsible for obesity because it is processed only by the liver, and here it can overload the ability of the liver to effectively process nutrients.
The effects of fructose on humans is difficult to assess because of the problems associated with controlling human diets. However, research using rodents has shown that fructose is likely the causative agent of insulin resistance in mammals. For example, one study1 investigated the effects of glucose or fructose at 35 % of the total calories in the diet on the insulin resistance displayed by rats. The insulin sensitivity was assessed using the euglycaemic clamp method, and the decrease in the requirement of glucose to maintain blood glucose levels was used as a measure of the resistance of glucose to enter cells. Following 4 weeks on the diets, the glucose infusion rate required to maintain blood glucose concentrations in the fructose fed rats decrease significantly. The authors noted that this response was found equally in both hepatic and peripheral tissues. In addition, the triglyceride concentrations became elevated in fructose eating rats.
These results suggest that fructose, but not glucose consumption may be a contributory factor in the development of insulin resistance in mammals. Evidence from human studies support these results and suggest that fructose induced insulin resistance is also relevant to man. The same authors have also demonstrated that sucrose can cause impairment of the action of insulin in rats when compared to a high starch diet. These results confirm that it is not the glucose moiety of sucrose that is the cause of this action, but the fructose moiety. Fructose is thought to lead to insulin resistance because it increases rates of de novo lipogenesis in the liver. The resulting lipids are stored in both liver and skeletal muscle where they may interfere with the insulin signal cascade which decreases the ability of insulin to stimulate glucose transport. This subsequently decreases the uptake of glucose from the plasma.
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