EFFECT OF CHRONIC PORTAL-HYPERTENSION ON GLUTAMINE TRANSPORT ACROSS RAT INTESTINAL BRUSH-BORDER AND BASOLATERAL MEMBRANES

Citation
Hm. Said et al., EFFECT OF CHRONIC PORTAL-HYPERTENSION ON GLUTAMINE TRANSPORT ACROSS RAT INTESTINAL BRUSH-BORDER AND BASOLATERAL MEMBRANES, The Journal of laboratory and clinical medicine, 122(1), 1993, pp. 64-68
Citations number
26
Categorie Soggetti
Medicine, Research & Experimental
ISSN journal
00222143
Volume
122
Issue
1
Year of publication
1993
Pages
64 - 68
Database
ISI
SICI code
0022-2143(1993)122:1<64:EOCPOG>2.0.ZU;2-0
Abstract
The present study examined the effect of chronic portal hypertension o n the intestinal transport of glutamine across the brush border membra ne (BBM) and the basolateral membrane (BLM) of the rat enterocyte. Chr onic portal hypertension was induced by partial portal vein ligation, and the results were compared with results in sham-operated rats. Tran sport studies were performed by using established techniques of isolat ed membrane vesicles. In chronic portal hypertensive rats, transport o f glutamine in BBM vesicles (BBMVs) exhibited significant inhibition i n the maximal velocity (V(max)) of both the Na+-dependent and the Na+- independent transport processes, with no significant changes in the ap parent Michaelis-Menten constant (K(m)) of the carrier systems. Simila rly, chronic portal hypertension caused a significant decrease in the V(max) of the Na+-dependent and the Na+-independent uptake processes i n 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 betwe en the portal hypertensive and sham-operated rats, because similar deg rees of enrichment and depurification of marker enzyme activities were seen in final vesicular preparations in the two rat groups. These res ults demonstrate that in chronic portal hypertension, glutamine transp ort across both poles of the enterocyte is impaired. At both the BBM a nd BLM domains, the impairment appears to be mediated via a decrease i n the number (and/or activity) of the glutamine carrier systems, with no changes in their affinity. The results also suggest that the impair ment of glutamine transport in chronic portal hypertension could lead to an impairment in normal energy requirement of the enterocyte and it s ability to function effectively.