In chickens, we have shown that intestinal absorption of
glucose via apical SGLT1 and basolateral GLUT2
transport systems is affected by dietary Na+; low-Na+
adapted birds show a dramatic reduction of glucose
transporters in both membranes in the rectum, an
intermediate response in the ileum and no effects in the
jejunum. We have now studied the effect of resalination of low-Na+
adapted chickens on glucose kinetics across SGLT1 (using α
-methyl-D-glucoside as substrate) and GLUT2 (using D-glucose) and on
the specific binding of phlorizin and cytochalasin B, respectively.
Twelve-week-old male Leghorn chickens were fed wheat and barley
with drinking water containing either 150 mM NaCl (high-Na+ group)
or 0.015 mM (low-Na+ group) for 14 days (serum aldosterone: 242 ± 6
pg ml-1 in the low-Na+ and 46 ± 4 pg ml-1 in the high-Na+ group). On
day 14, the low-Na+ group was either resalinated with an oral dose of
NaCl (9 g (kg body wt)-1) or switched to the high-Na+ condition, for 1
week. Serum aldosterone measured 4 h, 1 day and 7 days after the
change in NaCl intake fell to between 30 and 39 pg ml-1. The changes in
apical α-methyl-D-glucoside and basolateral D-glucose transport
observed in the ileum and rectum of low-Na+ adapted animals were
completely reversed by resalination within 4 h of NaCl administration
to the level of values observed for high-Na+ adapted birds. The good
correlation between the α-methyl-D-glucoside and D-glucose Vmax and
the SGLT1 and GLUT2 density, respectively, supports the view that the
increase in apical and basolateral hexose transport found in the ileum
and rectum of both groups of resalinated birds is due to an increase in
the number of protein transporters. The rapid changes in the number of
glucose transporters observed suggest that the target of the regulatory
signal(s) involved are the mature enterocytes present in the villi rather
than the developing enterocytes in the crypt.