Objectives: Six enzyme activities are needed to digest starch to absorbable free glucose; 2 luminal α-amylases (AMY) and 4 mucosal maltase-glucoamylase (MGAM) and sucrase-isomaltase (SI) subunit activities are involved in the digestion. The AMY activities break down starch to soluble oligomeric dextrins; mucosal MGAM and SI can either directly digest starch to glucose or convert the post-α-amylolytic dextrins to glucose. We hypothesized that MGAM, with higher maltase than SI, drives digestion on ad limitum intakes and SI, with lower activity but more abundant amount, constrains ad libitum starch digestion.
Methods: Mgam null and wild-type (WT) mice were fed with starch diets ad libitum and ad limitum. Fractional glucogenesis (fGG) derived from starch was measured and fractional gluconeogenesis and glycogenolysis were calculated. Carbohydrates in small intestine were determined.
Results: After ad libitum meals, null and WT had similar increases of blood glucose concentration. At low intakes, null mice had less fGG (P = 0.02) than WT mice, demonstrating the role of Mgam activity in ad limitum feeding; null mice did not reduce fGG responses to ad libitum intakes demonstrating the dominant role of SI activity during full feeding. Although fGG was rising after feeding, fractional gluconeogenesis fell, especially for null mice.
Conclusions: The fGNG (endogenous glucogenesis) in null mice complemented the fGG (exogenous glucogenesis) to conserve prandial blood glucose concentrations. The hypotheses that Mgam contributes a high-efficiency activity on ad limitum intakes and SI dominates on ad libitum starch digestion were confirmed.
*USDA/ARS Children's Nutrition Research Center and the Department of Pediatrics, Baylor College of Medicine, Houston, TX
†Whistler Center for Carbohydrate Research, Department of Food Sciences, Purdue University, West Lafayette, IN.
Address correspondence and reprint requests to Buford L Nichols, Children's Nutrition Research Center, 1100 Bates St, Houston, TX 77030 (e-mail: email@example.com).
Received 10 November, 2012
Accepted 25 June, 2013
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This study was supported in part by research funds from USDA ARS 6250-51000-052 including the MS and the Mouse Metabolic Research Units. The Comprehensive Lab Animal Monitor system was supported by NIH grant number S10RR024629. M.D.-S. was supported by the Post-Doctoral Fellowship Program of Instituto Nacional de Perinatología, México, D.F. México. This investigation was part of the Texas Medical Center Digestive Diseases Center (NIH DK58338) and Whistler Center for Carbohydrate Research (internal funding). The other authors report no conflicts of interest.