Proposed Mechanism by which Dietary Carbohydrates Glycemic Index Influence Insulin Resistance

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Adipocyte metabolism is central to the pathogenesis of insulin resistance and dietary carbohydrates influence adipocyte function. The previous simplistic view that insulin resistance resulted from the down-regulation of the insulin receptors in response to hyperinsulinemia is being replaced by the hypothesis that high circulating NEFA levels both impair insulin action and reduce pancreatic fi cell secretion. It is plausible that low glycemic index carbohydrates reduce insulin resistance by their ability to reduce adipocyte NEFA release. There is evidence of a loss of suppression of hormone-sensitive lipase (HSL), an enzyme that breaks down triglyceride to free fatty acids and glycerol, to small physiological amounts of insulin and, to a lesser extent, insulin insensitivity of lipoprotein lipase. HSL is normally very sensitive to small increases in insulin levels and is totally suppressed at much lower concentrations than those required for glucose uptake. In insulin-resistant subjects, HSL is less sensitive to small changes in insulin levels and adipocyte NEFA release is increased. A relationship between increased adipo-cyte NEFA release and insulin resistance has been shown in subjects with coronary heart disease. The metabolic consequences of increased circulating NEFA are multiple and are beyond the scope of this review, but they include adverse lipoprotein and coagulation changes and have been reported to affect insulin secretion and have a lipotoxic effect on the fi cell. Accumulation of triglyceride within the fi cell also impairs insulin secretion.

Many of the metabolic benefits associated with low glycemic index carbohydrates can be attributed to their ability to reduce adipocyte NEFA release. Low glycemic index foods have been consistently shown to reduce insulin resistance, and animal studies have shown that improvements in fat and muscle insulin sensitivity are accompanied by decreases in fatty acid synthatase activity, adipocyte size, and lipid storage. Although human studies have shown that low glycemic index diets consumed for 3 weeks increase adipocyte insulin sensitivity, no direct effect on adipocyte metabolism has been identified.

Low glycemic index diets attenuate the insulin response for approximately 4h postprandially. This slightly high postprandial insulin is insufficient to affect glucose transport but does suppress the insulin-sensitive enzyme, HSL, and thus ensures prolonged suppression of postprandial NEFA output. The ability of low glycemic carbohydrates to do this is in stark contrast with high glycemic diets that can cause an elevation of NEFA release post-prandially by stimulating the counterregulatory hormones, as discussed previously. Low glycemic meals taken in the evening can effectively suppress circulating NEFA concentrations and hepatic glucose output throughout the night. These metabolic effects are predicted to promote insulin sensitivity.

Our own work has shown that insulin-resistant adults with a history or who are at risk of CHD improve their adipocyte insulin sensitivity after consuming a low glycemic index diet for 3 weeks and their circulating NEFA levels decline. These human studies complement animal work showing that low glycemic index diets improve insulin sensitivity by modulating adipocyte metabolism.

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