Resistant starch is the fraction of starch not digested enzymatically in the small intestine. Resistant starch is considered a form of dietary fibre bacause it passes to the colon where bacterial degradation causes its conversion to short-chain fatty acids (SCFA). These fatty acids (mainly acetate and propionate) are then absorbed where they are used as a source of energy. Before the mid 1980s all starch was considered to be digested and so nutritionally resistant starch is novel and its physiological implications are not fully understood. The amount of resistant starch in foods depends on the processing, preparation and storage of the food, with some starch sources having more resistant starch than others. For example, potato starch is almost completely resistant to digestion, but heating gelatinises the starch allowing digestion. Cooling the potato again reverses this gelatinisation and causes around 12% of the starch to become resistant.
Because certain types of dietary fibre are beneficial to glycaemic control, and because resistant starch is a type of fibre, researchers1 have investigated the effects of resistant starch on postprandial glucose metabolism in 10 healthy individuals. Subjects were fed either 50g of gelatinised starch containing no resistant starch, or 50g of raw potato starch containing 54% resistant starch, both in an artificially sweetened syrup. Following consumption of the resistant starch meal, plasma concentrations of glucose, lactate, insulin, gastric inhibitory peptide (GIP), glucagon-like peptide-1 (GLP-1) and adrenaline were significantly lower compared to the resistant starch free meal. The reductions in GIP and GLP-1 mirrored the reduction in insulin suggesting that the cause was the lower amount of carbohydrate in the resistant starch meal. The subjects reported lower satiety scores with the resistant starch meal compared to the resistant starch free meal.
Therefore while resistant starch appears to allow better control of blood glucose, it also may not provide a feeling of fullness associated with digestible starch food. Generally, soluble and insoluble dietary fibre has been shown to increase satiety, whereas resistant starch may not have this property. This may result because the satiety effects of food derives from the interaction of glucose or signals from glycogen stores to glycol-sensitive parts of the hypothalamus and feedback from insulin. The lower levels of blood sugar and insulin seen following the resistant starch meal may therefore be interpreted by the brain as evidence of insufficient energy, which in turn fails to decrease appetite. Because the resistant starch is converted to SCFA and these are absorbed and used for energy production, it is tempting to speculate that long-term satiety would increase if resistant starch was consumed regularly.
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