Location: Children's Nutrition Research CenterTitle: Regulatory role of mucosal maltase-glucoamylase in starch digestion and glucose homeostasis) Author
Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract only
Publication Acceptance Date: 4/6/2010
Publication Date: 4/6/2010
Citation: Diaz-Sotomayor, M., Avery, S.E., Chacko, S.K., Quezada-Calvillo, R., Yan, L., Hamaker, B.R., Nichols, B.L. 2010. Regulatory role of mucosal maltase-glucoamylase in starch digestion and glucose homeostasis [abstract]. Journal of Federation of American Societies for Experimental Biology. 24:231.8. Interpretive Summary:
Technical Abstract: Slower rates of starch digestion by sucrase-isomaltase (Si) in Mgam null mice may fail to regulate gluconeogenesis (GNG). Mgam nulls have 40% reduction of glucose production from starch. The aim of this study was to measure glycemic index and rate of gluconeogenesis (fGNG) as fraction of total glucose appearance (Ra) and glucogenesis from starch (MPE) by Mgam null and WT mice. Groups of 4–8 null or WT mice were on low 13C-diet and trained to feed from 12–13 h after previous feed (hAF). D2O was given IP at 2 hAF. 13C-enriched starch was fed from 12–12.5 or 13 hAF and intake weighed. Blood was obtained by tail nicking at 5, 12, 12.5, 13, 14, and 16 hAF and decapitation at 14 or 16 hAF. Blood glucose was by glucometer and spotted on filter paper for MS. Glucose was derivatized as penta-acetate and run by GC-C-IRMS for 13C-glucose (MPE) and for 2H-C5-glucose (fGNG) enrichments by GC-MS. Body D2O dilution was by IRMS. Inverse correlation between MPE and fGNG was found (R-Sq 86%). At 14 hAF 0.5, but not 1.0 g, feeds, WT MPE exceeded null (p 0.02). Fasted fGNG averaged 71% and when fed null fell to 30% and WT to 20% (p 0.03). 1 gm intakes increased MPE only of null consistent with known in-vitro substrate inhibition of Mgam. Mgam activity regulates fGNG and is critical for starch digestion at snacking (0.5 g) but not at feasting (1 g) intakes. Mgam deficiency was compensated by increased fGNG. Glycemic index was regulated both by MPE and GNG pathways.