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Enteral glutamine: a novel mediator of PPARγ in the postischemic gut
Author(s) -
Ban Kechen,
Kozar Rosemary A.
Publication year - 2008
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.1107764
Subject(s) - glutamine , enteral administration , biology , arginine , peroxisome proliferator activated receptor , inflammation , receptor , medicine , endocrinology , parenteral nutrition , biochemistry , immunology , amino acid
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 γ. 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.