Glutamine signaling in intestinal cells.

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.

• Authors: M Rhoads
• Journal: JPEN. Journal of parenteral and enteral nutrition (JPEN J Parenter Enteral Nutr) 1999 Sep-Oct Vol. 23 Issue 5 Suppl Pg. S38-40 ISSN: 0148-6071 [Print] United States
• PMID: 10483892 (Publication Type: Journal Article, Review)

Chemical References

• Glutamine
• Sodium Chloride
• Mitogen-Activated Protein Kinases

Topics

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