Resistant starch, also known as dietary fibre, represents the fraction of carbohydrate intake that contains glycosidic bond types that result in incomplete hydrolysis by human digestive enzymes. Such carbohydrate was once considered to be important to health solely because it added bulk to foods and aided gut transit. However, advances in the nutritional sciences have revealed that resistant starch plays a far more important role in human metabolism than was once thought. It is now known that resistant starch passes to the colon where gut bacteria fermentation causes the formation of short chain fatty acids (SCFA), such as propionate, butyrate and acetate. These SCFAs are then absorbed where they provide the host with energy over an extended period. Following consumption, resistant starch also forms a gel, and this may decrease the rate of glucose absorption, through creation of a barrier in the unstirred layer of the brush boarder.
Resistant starches are therefore potentially useful tools in controlling blood sugar and maintaining constant energy in individuals with blood sugar disorders. This may explain their glycaemic effects in clinical studies investigating benefits to diabetes, metabolic syndrome and obesity. Naturally occurring resistant starch is found in high fibre foods such as beans, oats and barley. However, artificially synthesised resistant starches are available commercially. Dextrins are low molecular weight carbohydrates produced by hydrolysis of starch. Some resistant dextrins have been manufactured and tested for their beneficial blood glucose and energy release properties. For example, researchers1 used a randomised, double-blind placebo controlled cross-over design study to investigate the effects of a resistant dextrin on 12 healthy men. Subjects ingested a normal breakfast containing either 50g of the resistant dextrin nutriose or 50g of the non-resistant maltodextrin, both followed by a normal lunch 5 hours later.
In this study both the resistant starch and maltodrextrin were derived from corn which is naturally rich in 13C, and so stable isotope analysis was used to assess the metabolic fate of the starch. Oxidation and fermentation rates were assess by measuring the 13CO2/H2 ratio in breath, and the appearance of glucose in the plasma was measured by the plasma 13C-glucose concentration. Analysis of the data showed that 13Cglucose appearance in plasma, and glycaemic and insulin responses to the resistant starch were significantly lower, compared to maltodextrin. This suggests that glucose from nutriose is more slowly released when compared to maltodextrin. In addition, H2 excretion was significantly elevated following consumption of nutriose, probably because fermentation in the colon was higher, compared to maltodextrin. The appearance of CO2 in the breath was significantly prolonged by consumption of the resistant starch, indicating a delayed oxidation.
Ghrelin is a hunger stimulating hormone secreted by the stomach, and plasma levels fall in relation to the energy content of a meal. Ghrelin was inhibited to a greater extent by maltodextrin compared to the resistant starch, which suggests that the resistant dextrin released energy more slowly thereby reducing the ghrelin signal more gradually. Non-esterified fatty acids in the plasma, a measure of the use of fatty acids as a fuel, were significantly higher in the resistant starch treatment, confirming the slower absorption of glucose to the plasma. Following lunch non-esterified plasma fatty acids decreased in both groups as would be expected following ingestion of a normal mixed meal. These results suggest that the dextrin nutriose shows a delayed absorption and prolonged oxidation pattern that may make it a useful tool in reducing the glycaemic load of those with blood sugar disorders.
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