Glutamine stimulates prostaglandin-sensitive Na(+)-H+ exchange in experimental porcine cryptosporidiosis.
OBJECTIVE
Recent studies of piglet cryptosporidiosis showed an injury-induced impairment of sodium-glucose cotransport and a prostaglandin-mediated inhibition of neutral NaCl absorption. Because glutamine has been shown to stimulate both neutral and electrogenic Na+ absorption, this study examined the mechanism of prostaglandin-mediated inhibition of NaCl absorption and the effect of glutamine on these processes.


METHODS
Ileal mucosa from control and infected pigs was mounted in Ussing chambers for flux studies or incubated with [14C]glutamine or [14C]-glucose for metabolism studies.


RESULTS
Glucose and glutamine induced equivalent increases, 2-2.5 microEq.cm-2.h-1, in Na+ absorption and short-circuit current in control ileum. Despite a reduction in villous surface area to one third of the control, glutamine enhanced both neutral and electrogenic Na+ absorption in the infected ileum by 3.5 +/- 0.5 microEq.cm-2.h-1, whereas glucose was only half as effective (P < 0.05). In addition, glutamine was oxidized to CO2 at rates three times those of glucose. Indomethacin enhanced, whereas amiloride, prostaglandin E2, and Cl-free solutions inhibited the glutamine-induced neutral Na+ transport.


CONCLUSIONS
Glutamine-stimulated neutral Na+ absorption is mediated by a prostaglandin-sensitive apical Na(+)-H+ exchange mechanism. The heightened Na(+)-H+ exchange and tissue oxidation of glutamine suggest that glutamine is superior to glucose for use in oral rehydration solutions.
Argenzio
R A
RA
Center for Gastrointestinal Biology, North Carolina State University, Raleigh.
Rhoads
J M
JM
Armstrong
M
M
Gomez
G
G
D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D002712:Chlorides / Q000378:metabolism; D003457:Cryptosporidiosis / Q000378:metabolism* / Q000473:pathology; D005947:Glucose / Q000378:metabolism / Q000494:pharmacology; D005973:Glutamine / Q000378:metabolism / Q000494:pharmacology*; D007082:Ileum / Q000473:pathology; D007213:Indomethacin / Q000494:pharmacology; D007413:Intestinal Mucosa / Q000473:pathology; D010084:Oxidation-Reduction; D011453:Prostaglandins / Q000494:pharmacology*; D012964:Sodium / Q000378:metabolism; D017923:Sodium-Hydrogen Exchangers / Q000037:antagonists & inhibitors / Q000378:metabolism*; D013552:Swine
D002712:Chlorides; D011453:Prostaglandins; D017923:Sodium-Hydrogen Exchangers; D005973:Glutamine; D012964:Sodium; D005947:Glucose; D007213:Indomethacin