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
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.