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J. Nutr. (February 4, 2009). doi:10.3945/jn.108.098434
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© 2009 American Society for Nutrition


Nutrition and Disease

Mucosal Maltase-Glucoamylase Plays a Crucial Role in Starch Digestion and Prandial Glucose Homeostasis of Mice1,2,3

Buford L. Nichols4,*, Roberto Quezada-Calvillo4,5, Clnamedia C. Robayo-Torres4, Zihua Ao6, Bruce R. Hamaker6, Nancy F. Butte4, Juan Marini4, Farook Jahoor4 and Erwin E. Sterchi7

4 USDA, Agricultural Research Service, Children's Nutrition Research Center and Department of Pediatrics, Baylor College of Medicine, Houston, TX, 77030-300 5 CIEP-Facultad de Ciencias Quimicas, Universidad Autonoma de San Luis Potosí, Zona Universitaria, San Luis Potosí, S.L.P., Mexico, 78360 6 Whistler Center for Carbohydrate Research and Department of Food Science, Purdue University, West Lafayette, IN 47907-2009 7 Institute of Biochemistry and Molecular Medicine, University of Berne, CH-3012 Berne, Switzerland

Starch is the major source of food glucose and its digestion requires small intestinal {alpha}-glucosidic activities provided by the 2 soluble amylases and 4 enzymes bound to the mucosal surface of enterocytes. Two of these mucosal activities are associated with sucrase-isomaltase complex, while another 2 are named maltase-glucoamylase (Mgam) in mice. Because the role of Mgam in {alpha}-glucogenic digestion of starch is not well understood, the Mgam gene was ablated in mice to determine its role in the digestion of diets with a high content of normal corn starch (CS) and resulting glucose homeostasis. Four days of unrestricted ingestion of CS increased intestinal {alpha}-glucosidic activities in wild-type (WT) mice but did not affect the activities of Mgam-null mice. The blood glucose responses to CS ingestion did not differ between null and WT mice; however, insulinemic responses elicited in WT mice by CS consumption were undetectable in null mice. Studies of the metabolic route followed by glucose derived from intestinal digestion of 13C-labeled and amylase-predigested algal starch performed by gastric infusion showed that, in null mice, the capacity for starch digestion and its contribution to blood glucose was reduced by 40% compared with WT mice. The reduced {alpha}-glucogenesis of null mice was most probably compensated for by increased hepatic gluconeogenesis, maintaining prandial glucose concentration and total flux at levels comparable to those of WT mice. In conclusion, mucosal {alpha}-glucogenic activity of Mgam plays a crucial role in the regulation of prandial glucose homeostasis.


* To whom correspondence should be addressed. E-mail: bnichols{at}bcm.tmc.edu.

Manuscript received 18 August 2008. Initial review completed 21 October 2008. Revision accepted 6 January 2009.







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