Effect of chronic portal hypertension on glutamine transport across rat intestinal brush border and basolateral membranes
Said, H.M.; Morgan, T.; Hoefs, J.
Journal of Laboratory and Clinical Medicine 122(1): 64-68
1993
ISSN/ISBN: 0022-2143 PMID: 8320492 Document Number: 413460
The present study examined the effect of chronic portal hypertension on the intestinal transport of glutamine across the brush border membrane (BBM) and the basolateral membrane (BLM) of the rat enterocyte. Chronic portal hypertension was induced by partial portal vein ligation, and the results were compared with results in sham-operated rats. Transport studies were performed by using established techniques of Isolated membrane vesicles. In chronic portal hypertensive rats, transport of glutamine in BBM vesicles (BBMVs) exhibited significant inhibition in the maximal velocity (V-max) of both the Na+-dependent and the Na+-independent transport processes, with no significant changes in the apparent Michaelis-Menten constant (K-m) of the carrier systems. Similarly, chronic portal hypertension caused a significant decrease in the V-max of the Na+-dependent and the Na+-independent uptake processes in intestinal BLM vesicles (BLMVs), with no change in the apparent K-m of the uptake systems. These changes in glutamine transport in BBMVs and BLMVs brought about by chronic portal hypertension are not due to differences in the relative purity of the vesicular preparations between the portal hypertensive and sham-operated rats, because similar degrees of enrichment and depurification of marker enzyme activities were seen in final vesicular preparations in the two rat groups. These results demonstrate that In chronic portal hypertension, glutamine transport across both poles of the enterocyte is impaired. At both the BBM and BLM domains, the impairment appears to be mediated via a decrease in the number (and/or activity) of the glutamine carrier systems, with no changes in their affinity. The results also suggest that the impairment of glutamine transport in chronic portal hypertension could lead to an impairment In normal energy requirement of the enterocyte and its ability to function effectively.