l-glutamine stimulates jejunal sodium and chloride absorption in pig rotavirus enteritis

Rotavirus enteritis is the leading cause of diarrhea in infants worldwide. A research priority of the World Health Organization is to develop oral rehydration solutions containing amino acids or other additives that will stimulate intestinal absorption more efficiently than the current glucose-based oral rehydration solutions. Glutamine is the principal metabolic fuel of the small bowel and a putative stimulator of mucosal repair. This report describes the transport response to mucosal l-glutamine following intestinal injury caused by porcine rotavirus. Peak symptoms and mucosal damage were observed 2–7 days after oral rotavirus inoculation. In vitro transport studies of the maximally injured region, the midjejunum (80% reduction in lactase), surprisingly, showed transport responses to l-glutamine (30 mmol/L) Sand l-alanine (30 mmol/L) that were similar qualitatively and quantitatively to those observed in control tissue. Subsequent application of mucosal d-glucose (30 mmol/L) caused additional stimulation of electrogenic Na(+) transport, but the response to glucose was blunted (P < 0.05) in the infected tissues. Glutamine and alanine enhanced Na(+) absorption to a similar degree (2–2.5 μEq · cm(−2) · h(−1)), but glutamine stimulated equal amounts of electrogenic and electroneutral NaC1 absorption, whereas alanine had no significant effect on net Cl(−) flux. Glutamine is a potentially useful substrate for investigation in oral rehydration solutions for infant diarrhea.