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Title: Maltase-glucoamylase: Mucosal regulator of prandial starch glucogenesis and complementary hepatic gluconeogenesis of mice

Author
item DIAZ-SOTOMAYOR, MARICELA - Children'S Nutrition Research Center (CNRC)
item QUEZADA-CALVILLO, ROBERTO - Children'S Nutrition Research Center (CNRC)
item AVERY, STEPHEN - Children'S Nutrition Research Center (CNRC)
item CHACKO, SHAJI - Children'S Nutrition Research Center (CNRC)
item YAN, LIKE - Purdue University
item HAMAKER, BRUCE - Purdue University
item NICHOLS, BUFORD - Children'S Nutrition Research Center (CNRC)

Submitted to: Gastroenterology
Publication Type: Abstract Only
Publication Acceptance Date: 5/1/2010
Publication Date: 5/1/2010
Citation: Diaz-Sotomayor, M., Quezada-Calvillo, R., Avery, S., Chacko, S., Yan, L., Hamaker, B.R., Nichols, B.L. 2010. Maltase-glucoamylase: Mucosal regulator of prandial starch glucogenesis and complementary hepatic gluconeogenesis of mice [abstract]. Gastroenterology. 138(Suppl.1):S-406-S-407.

Interpretive Summary:

Technical Abstract: It was hypothesized that the slower rate of starch digestion by residual sucraseisomaltase (Si) maltase failed to fully regulate gluconeogenesis. In the present study the rate of gluconeogenesis was measured directly (J Appl Physiol 104: 944-951, 2008) and compared with exogenous glucose derived from starch digestion by Mgam (Maltase-glucoamylase) null and WT (Wild Type) mice. The Mgam null and WT mice have been previously published (J. Nutr.137: 1725-1733, 2007). The null mice with only Si have a 58% reduction in jejunal glucogenic activity. The experimental mice were on a low 13C-diet (MPE% (mol percent enrichment) 0.003+/-0.003) from conception. At 10 wks age, they were trained to feed from 16-22 h after the previous feeding in CLAMS unit. D2O (deuterium water) was given IP at 2 h. 13C-enriched starch (MPE%0.1 +/- 0.003) was fed at 12 h after the previous feed and intake weighed. Blood was obtained from tails at 5, 12, 12.5, 13, and 14 h and by decapitation at 14 and 16 h., Blood glucose was measured by glucometer and spotted on filter paper for MS (mass spectrometry) analysis. Glucose was derivatized as penta-acetate and run by GC-C-IRMS (gas chromatography combustion isotope ratio mass spectrometry) for 13C-glucose (MPE%; glucogenesis) and for 2HC5-glucose (fGNG; fractional gluconeogenesis) by GC-MS (gas chromatography mass spectrometry). Body D2O dilution was by IRMS. The fGNG of all fasting mice was constant from 5-16 h and in all fed mice was steady from 14-16 h. Unfed control fGNGs were constant between 5-16 h. The 12-16 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.