Glutamine signaling in intestinal cells

JPEN J Parenter Enteral Nutr. 1999 Sep-Oct;23(5 Suppl):S38-40. doi: 10.1177/014860719902300510.

Abstract

Glutamine (Gln) is a "competence factor" necessary for intestinal cell proliferation, intestinal fluid/electrolyte absorption, and mitogenic response to growth factors. Gln deprivation produces apoptosis. Gln stimulation of quiescent cells produces immediate-early gene expression and MAP kinase activation. However, EGF signals more powerfully through MAPKs than Gln. Interestingly, EGF-stimulated mitogenesis is ineffective in the absence of Gln. In the intact intestinal epithelia in vivo, Gln has powerful effects on absorption of sodium and chloride. Gln-stimulated absorption is greater than and additive to glucose-stimulated absorption in cryptosporidial enteritis. In the piglet ileum, Gln metabolism stimulates apical amiloride-inhibitable Na+/H+ exchange. Although one might predict powerful effects of oral Gln on absorption in babies with diarrhea, 3 clinical trials to date (one published) have not shown an advantage of Gln-supplemented oral rehydration solutions (ORS) compared to standard glucose ORS. Severely dehydrated subjects have not been studied. More important effects of Gln treatment may be seen with (1) co-administration with a growth factor and (2) in patients with severe intestinal damage, such as protracted diarrhea of infancy or AIDS enteropathy.

Publication types

  • Review

MeSH terms

  • Animals
  • Cell Division
  • Glutamine / physiology*
  • Humans
  • Intestinal Absorption
  • Intestinal Mucosa / metabolism*
  • Intestines / enzymology
  • Intestines / physiology*
  • Mitochondria / drug effects
  • Mitochondria / physiology
  • Mitogen-Activated Protein Kinases / metabolism
  • Sodium Chloride / metabolism

Substances

  • Glutamine
  • Sodium Chloride
  • Mitogen-Activated Protein Kinases