Reduced glycemic response to starch feeding of Mgam null mice is buffered by increased endogenous gluconeogenesis

Abstract

Six digestive enzymes are required to break down starch polymers to free glucose before intestinal absorption. Understanding of the contribution of individual digestive enzymes on this process may provide a new strategy to manage prandial glucose.ObjectiveDetermine the effect of poor starch digestion causing by the absence of maltase‐glucoamylase (Mgam) on glycemia response.MethodMgam null mice and wild type (WT), 4 each, were fasted for 12 h and then fed normal corn starch. They were sacrificed at 16 h. Timed blood glucose and total free glucose, soluble oligomers, and starch residues remaining in the small intestine (SI) were measured.ResultGlycemic response to feeding in the 2 genotypes of mice was not different. However, after 4 h the persistence of indigested carbohydrates in SI of null mice (60%) was higher than WT (30%). Null and WT mice had similar amylolysis activity (oligomers/residual starch), but null mice had lower glucosidase activity, (free glucose/ residual starch: 0.4 null and 0.9 WT mice).ConclusionIt is known that Mgam null mice have lower glucosidase activity in vivo, and in vitro. Here we report that WT was associated with more complete lumenal digestion of granular starch, but the blood glucose response of null mice was fully compensated by gluconeogenesis. Reduced starch glucogenesis in null mice is buffered by endogenous glucose production which obscures the prandial glycemia response.Grant Funding Source: USDA ARS 6250–51000‐052 and the internal funding from Whistler Center for Carbohydrate Research at Purdue Univ.