Gastric emptying may be an important determinant of the glycaemic effect of food. Because lower a glycaemic load is associated with protection from weight gain, diabetes and cardiovascular disease, nutritional factors that can inhibit or delay gastric emptying are of interest to nutritional researchers. Release of the incretin hormones glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotrophic hormone (GIP) are impaired in diabetes. While their release is thought to account for up to half of the insulin response to a meal, they also play a role in delaying gastric emptying and reducing appetite, and may decrease energy intake. Some evidence suggest that the incretins are stimulated by either the taste of carbohydrate foods or activation of the sodium-glucose cotrasporter 1 (SGLT1) in the small intestine. This suggests that different sugars may have differing effects on incretin release and that some sugars may have beneficial effects if incorporated in the diet.
Researchers1 have investigated the effects three sugars (40g glucose, 40g tagatose/isomalt mixture, 40g 3-O-methylglucose) and a sweetener (60g sucralose) on incretin release in 10 healthy subjects. The treatments were consumed before a potato meal which was 13C labelled. The results showed that all of the calorific sugars (glucose, tagatose/isomalt mixture, 3-O-methylglucose) stimulated GLP-1 to a greater extent than the artificial sweetener sucralose. Both the tagatose/isomalt mixture and 3-O-methylglucose inhibited gastric emptying (glucose was not significant due to a large standard deviation) when compared to the artificial sweetener sucralose. These results suggest that the sweet taste of sucralose was not the reason for the effects. Both glucose and 3-O-methylglucose stimulated incretin release prior to ingestion of the potato meal whereas the tagatose/isomalt mixture and sucralose treatment did not. Postprandially, glucose created the largest GLP-1, plasma glucose and plasma insulin response of all of the treatments.
Because 3-O-methyl glucose is a substrate for SGLT-1 but is not metabolised in humans, it may be that SGLT-1 is involved in the stimulation of incretin release. While ingestion of the sugars cause delayed gastric emptying, GLP-1 release and reduced appetite, ingestion of sucralose did not. This suggests that carbohydrate in the gut, and not the sweet taste, is the likely trigger for incretin release. The authors picked the four sugars because of their matched sweetness rating, however, they could not be matched for viscosity or osmolarity, and so these variables may part in stimulation of incretins. Ingestion of non-metabolised substrates for SGLT-1 may be effective at regulating appetite and could be useful in weight control or in modulation of blood sugar disorders. The greater rise in plasma glucose and insulin following glucose ingestion is likely a reflection that the insulinotrophic effects of the incretins are glucose dependent.
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