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Contribution of Villous Atrophy to Reduced Intestinal Maltase in Infants With Malnutrition

Nichols, Buford L.*; Nichols, Veda N.*; Putman, Margaret*; Avery, Stephen E.*; Fraley, J. Kennard*; Quaroni, Andrea†; Shiner, Margot‡¶; Sterchi, Erwin E.§; Carrazza, Francisco R.∥

Journal of Pediatric Gastroenterology & Nutrition: May 2000 - Volume 30 - Issue 5 - pp 494-502
Original Articles

Background: It has been known for many years that small intestinal maltase activities are reduced in malnourished infants and in other patients with villous atrophy. The recent availability of human maltase-glucoamylase cDNA provides the opportunity to test the hypothesis that villous atrophy accounts for the reduced maltase enzyme activity in malnourished infants.

Methods: Mucosal biopsy specimens obtained for clinical evaluation of malnourished infants with poor responses to refeeding were examined by quantitative methods for enzyme activity and mRNA levels.

Results: Maltase activity and maltase-glucoamylase mRNA were reduced (approximately 45% of normal). When maltase-glucoamylase message was normalized to villin message, a structural protein expressed only in enterocytes, a preservation of maltase messages in surviving enterocytes was documented. The luminal glucose transporter–villin message was also preserved.

Conclusions: The loss of maltase-glucoamylase message paralleled the reduction in villin message and degree of villous atrophy. The reduced maltase-glucoamylase message also paralleled sucrase-isomaltase message, previously found to be decreased in proportion to villous atrophy of malnourished infants. The data directly demonstrate, for the first time, that the terminal steps of starch 1-4 starch digestion and sucrase-isomaltase 1-6 starch digestion are decreased in malnourished infants, secondary to villous atrophy. These data in prior and present reports suggest that mechanisms underlying the chronic villous atrophy of malnutrition should be a priority for investigations in malnourished infants with slower than expected weight gain during refeeding.

*U.S. Department of Agriculture/Agriculture Research Service, Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine and Texas Children's Hospital, Houston, Texas; †Cornell University, Ithaca, New York; ‡Department of Pediatric Gastroenterology, Sackler Medical School, Assaf Harofeh Hospital, Tel Aviv University, Tel Aviv, Israel; §Institute for Biochemistry and Molecular Biology of the University of Bern, Bern, Switzerland; ∥Departamento de Pediatria, Instituto da Criança, Hospital das Clinicas da Faculdade de Medicina, Universidade de São Paulo, Sãao Paulo, Brazil

Received October 6, 1999;

revised February 2, 2000; accepted February 7, 2000.

¶Deceased July 31, 1998.

Address correspondence and reprint requests to Buford L. Nichols, MD, USDA Children's Nutrition Research Center, Baylor College of Medicine, 1100 Bates Street, Houston, TX 77030-2600.

© 2000 Lippincott Williams & Wilkins, Inc.