Glutamine signaling in intestinal cells.
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.
Rhoads
M
M
Department of Pediatrics, University of North Carolina at Chapel Hill, 27599, USA.
D000818:Animals; D002455:Cell Division; D005973:Glutamine / Q000502:physiology*; D006801:Humans; D007408:Intestinal Absorption; D007413:Intestinal Mucosa / Q000378:metabolism*; D007422:Intestines / Q000201:enzymology / Q000502:physiology*; D008928:Mitochondria / Q000187:drug effects / Q000502:physiology; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D012965:Sodium Chloride / Q000378:metabolism
D005973:Glutamine; D012965:Sodium Chloride; D020928:Mitogen-Activated Protein Kinases