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Originally published online as doi:10.1189/jlb.1107764 on April 7, 2008

Published online before print April 7, 2008
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(Journal of Leukocyte Biology. 2008;84:595-599.)
© 2008 by Society for Leukocyte Biology

Enteral glutamine: a novel mediator of PPAR{gamma} in the postischemic gut

Kechen Ban and Rosemary A. Kozar1

Department of Surgery, University of Texas Health Science Center of Houston, Houston, Texas, USA

1 Correspondence: Department of Surgery, University of Texas Health Science Center of Houston, 6431 Fannin, MSB 4.284, Houston, TX 77030, USA. E-mail: rosemary.a.kozar{at}uth.tmc.edu

ABSTRACT

Early enteral nutrition supplemented with glutamine, arginine, omega-3 fatty acids, and nucleotides has been shown to decrease infection complications in critically injured patients. Concern has been raised, however, that under conditions of hyperinflammation, these diets may be injurious through the induction of inducible NO synthase by enteral arginine. In a rodent model of gut ischemia/reperfusion, inflammation and injury are intensified by enteral arginine and abrogated by glutamine. These findings correlate with the degree of metabolic stress imposed upon the gut by hypoperfusion. Glutamine is metabolized by the gut and therefore, can contribute back energy in the form of ATP, whereas arginine is a nonmetabolizable nutrient, using but not contributing energy. Recent data suggest that one of the molecular mechanisms responsible for the gut-protective effects of enteral glutamine is the activation of peroxisome proliferator-activated receptor {gamma}. This anti-inflammatory transcription factor belongs to the family of nuclear receptors, plays a key role in adipocyte development and glucose homeostasis, and has been recognized as an endogenous regulator of intestinal inflammation. Preliminary clinical studies support the use of enteral glutamine in patients with gut hypoperfusion.

Key Words: gut ischemia/reperfusion • IEC-6 cells • arginine • peroxisome proliferator response element




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