Increasingly is it being shown that the glycaemic response following a meal is a significant contributor to the risk of disease. Meals or foods that produce high glycaemic responses are now thought to contribute to the development of insulin resistance although the exact mechanism by which this happens in not fully understood. One possibility is that the rapid rise in blood sugar following a meal results in a conditions of nutrient overload, whereby the glucose overloads the cells of the body with energy. This energy then passess down the main energy producing pathways and the resulting reducing equivalents enter the electron transport chain where they overload it. This generates free radicals that overwhelm the defences of the cell and this generates oxidative stress. This oxidative stress may interfere with the insulin signal cascade and lead to the development of insulin resistance. Low glycaemic index foods may therefore protect from disease through limiting nutrient overload.
The glycaemic index is a common measure of the rate at which certain carbohydrate foods are digested and the subsequent glucose absorbed to the blood. However, the glycaemic response to a meal is far more complex than is described in the glycaemic index tables and many factors can influence the rate of glucose absorption to the blood. Many studies have compared various foods in order to understand the way in which they contribute to postprandial glycaemia. Often this has involved the comparison of simple sugars. For example, in one study1, researchers compared the glycaemic response to isomaltose and sucrose. Both isomaltose and sucrose are composed of a glucose molecule linked to a fructose molecule, but with the former having a glycaemic index of 32, while the latter has a glycaemic index of 65. The difference in the postprandial glycaemia between the two compounds is likely due to the different type of glycosidic bond joining the glucose and fructose moieties (isomaltose has an α-(1-6)-linkage; sucrose has an α-(1-4)-linkage).
The results of the study showed that the glycaemic response of isomaltose was prolonged for 50 min compared to sucrose. With isomaltose ingestion the mean plasma insulin, C-reactive protein, glucagon and glucose-dependent insulinotropic peptide (GIP) concentrations were 10 to 23 % lower in the isomaltose treatment compared to the sucrose treatment. The isomaltose treatment however resulted in a 64 % higher plasma concentration of glucagon-like peptide 1 (GLP-1; a potent suppressor of glucagon release) compared to the sucrose treatment. This suggests that the glucagon to insulin ratio following the isomaltose treatment was significantly lower, resulting in a suppression of endogenous glucose production, which further suppressed plasma glucose levels. Therefore the appearance of plasma glucose may be suppressed with isomaltose ingestion due to reductions in absorption rate, reductions in the production of endogenous glucose, as well as higher uptake of glucose by the liver.
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