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Am J Physiol Gastrointest Liver Physiol 275: G1259-G1265, 1998;
0193-1857/98 $5.00
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Vol. 275, Issue 6, G1259-G1265, December 1998

Mechanism of inhibition of Na+-bile acid cotransport during chronic ileal inflammation in rabbits

U. Sundaram1, S. Wisel1, S. Stengelin2, W. Kramer2, and V. Rajendran3

1 Division of Digestive Diseases, Departments of Medicine and Physiology, Ohio State University School of Medicine, Columbus, Ohio 43210; 2 Hoechst Marion Roussel, D-65926 Frankfurt, Germany; and 3 Yale University School of Medicine, New Haven, Connecticut 06520

In the chronically inflamed ileum, unique mechanisms of alteration of similar transport processes suggest regulation by different immune-inflammatory mediator pathways. In a rabbit model of chronic ileitis, we previously demonstrated that Na+-glucose cotransport was inhibited by a decrease in the cotransporter numbers, whereas Na+-amino acid cotransport was inhibited by a decrease in the affinity for the amino acid. In this study, we demonstrated that Na+-bile acid cotransport was reduced in villus cells from the chronically inflamed ileum. In villus cell brush-border membrane vesicles from the chronically inflamed ileum, Na+-bile acid cotransport was reduced as well, suggesting a direct effect at the cotransporter itself. Kinetic studies demonstrated that Na+-bile acid cotransport was inhibited by both a decrease in the affinity as well as a decrease in the maximal rate of uptake of the bile acid. Analysis of steady-state mRNA and immunoreactive protein levels of the Na+-bile acid cotransporter also demonstrated some reduction during chronic ileitis. Thus, in the chronically inflamed ileum, the mechanisms of inhibition of Na+-glucose, Na+-amino acid, and Na+-bile acid cotransport are different. These data suggest that different cotransporters are uniquely altered either secondary to their intrinsic differences or by different immune-inflammatory mediators during chronic ileitis.

inflammatory bowel disease; intestinal nutrient absorption; immune regulation of nutrient transport; sodium-potassium-adenosinetriphosphatase; bile acid absorption


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