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Department of Animal Science and Faculty of Nutrition, Texas A&M University, College Station, TX 77843-2471
The early-weaned pig develops intestinal atrophy and provides a readily accessible animal model for determining the role of dietary supplementation of glutamine (Gln, a major fuel for enterocytes) in preventing intestinal damage. Three experiments were conducted to determine the stability of dietary Gln in the acidic part of the gastrointestinal tract using pigs surgically fitted with a T-cannula in mid-duodenum (Exp. 1), and the effects of dietary Gln supplementation on the villus height and lamina propria depth of duodenum and jejunum (Exp. 2) as well as growth performance (Exp. 3) of pigs weaned at 21 d of age. Postweaning pigs were fed for 14 d com- and soybean meal-based diets supplemented with 0.0, 0.2, 0.6 or 1.0% free L-Gln. Dietary Gln was not subject to measurable acid hydrolysis in the stomach and upper part of duodenum and was substantially available for the small intestine for metabolic utilization. Glutamine supplementation (1.0%) prevented jejunal atrophy (as indicated by villus height) during the first week postweaning and increased the gain:feed ratio (an indicator of growth performance) by 25% during the second week postweaning. Glutamine supplementation (1.0%) increased plasma concentrations of aspartate, glutamate and alanine and reduced the extent to which plasma taurine concentration fell in postweaning pigs. These results provide an experimental basis for enteral use of Gln in swine production and clinical nutrition to prevent intestinal epithelial damage.
KEY WORDS: glutamine supplementation intestinal morphology pigs
1 Supported by funds from Ajinomoto, Inc. (Tokyo, Japan) and by Hatch projects #8200 and #6601 from the Texas Agricultural Experiment Station.
2 The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 USC section 1734 solely to indicate this fact.
3 To whom correspondence should be addressed.
Manuscript received 26 March 1996. Revision accepted 9 July 1996.
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