|DIAZ-SOTOMAYOR, MARICELA - Children'S Nutrition Research Center (CNRC)|
|AVERY, STEPEN - Children'S Nutrition Research Center (CNRC)|
|CHACKO, SHAJI - Children'S Nutrition Research Center (CNRC)|
|QUEZADA-CALVILLO, ROBERTO - Children'S Nutrition Research Center (CNRC)|
|NICHOLS, BUFORD - Children'S Nutrition Research Center (CNRC)|
Submitted to: Journal of Pediatric Gastroenterology and Nutrition
Publication Type: Abstract Only
Publication Acceptance Date: 11/1/2009
Publication Date: 11/1/2009
Citation: Diaz-Sotomayor, M., Avery, S.E., Chacko, S.K., Quezada-Calvillo, R., Nichols, B.L. 2009. Maltase-glucoamylase: Mucosal regulator of prandial starch glucogenesis and complimentary hepatic gluconeogenesis of mice [abstract]. Journal of Pediatric Gastroenterology and Nutrition. 49(Suppl.1):E26.
Technical Abstract: In previous studies we have shown that maltase-glucoamylase (Mgam) is required for efficient starch digestion and insulin response to starch feeding. It was hypothesized that the slower rate of starch digestion by residual sucrase-isomaltase (Si) maltase failed to regulate gluconeogenesis. Here, rate of fractional gluconeogenesis (fGNG) was measured directly (J Appl Physiol 2008;104:944–951) and compared with exogenous glucose derived from starch digestion by Mgam null and WT mice. The mice have been previously published (J Nutr 2007;137:1725–1733). The null mice with only Si have a 58% reduction in jejunal glucogenic activity. The experimental mice were on a low 13C-diet (glucose MPE% 0.003+/-0.003) from conception. At 10 wks age they were trained to feed from 18–22 h in a CLAMS unit. D2O was given IP at 02 h. 13C-enriched starch (MPE% 0.1+/-0.003) was fed from 18–22 h and intake weighed. Blood was obtained from tails at 11, 18, and 20 h and by decapitation at 22 h. Blood glucose was measured by glucometer and spotted on filter paper for MS analysis. Glucose was derivitized as penta-acetate and run by GC CIRMS for 13C-glucose (MPE%; glucogenesis) and deuterium enrichment in glucose by GC-MS (fGNG). Deuterium enrichment in body water was measured by IRMS. The fGNG of fasting mice was constant from 11–18 h and in fed mice was steady from 20–22 h. The 11–18 h fGNG in all fasted experimental mice averaged 71% and fell when fed; null mice dropped to 30% and WT to 20% fGNG (by genotype, P=0.000). An inverse correlation between glucogenesis (MPE%) and gluconeogenesis (fGNG) was found (R-Sq 86%). There is a homeostatic complementarily between intestinal glucogenesis from starch and hepatic gluconeogenesis. Mgam plays a crucial role in starch digestion and determines rate of exogenous glucose flux which results in prandial suppression of endogenous glucose flux.