Vol. 277, Issue 4, E750-E759, October 1999
Increased intracellular localization of brain GLUT-1
transporter in response to ethanol during chick
embryogenesis
F. M.
Carver1,
I. A.
Shibley Jr.1,
D. S.
Miles1,
J. S.
Pennington2, and
S. N.
Pennington1,3
Departments of 1 Biochemistry,
3 Pediatrics, and
2 Comparative Medicine, School
of Medicine, East Carolina University, Greenville, North Carolina 27858
Fetal exposure to ethanol is associated with
growth retardation of the developing central nervous system. We have
previously described a chick model to study the molecular mechanism of
ethanol effects on glucose metabolism in ovo. Total
membrane fractions were prepared from day
4, day 5, and
day 7 chick embryos exposed in ovo to
ethanol or to vehicle. By Western blotting analysis, ethanol exposure
caused a mean 7- to 10-fold increase in total GLUT-1 and a 2-fold
increase in total GLUT-3. However, glucose uptake by ethanol-treated
cells increased by only 10%. Analysis of isolated plasma (PM) and
intracellular (IM) membranes from day
5 cranial tissue revealed a mean 25% decrease in
GLUT-1 in the PM and a 66% increase in the IM in the ethanol group vs.
control. The amount of PM GLUT-3 was unchanged but that of IM GLUT-3
was significantly decreased. The data suggest that GLUT-3 cell surface expression may be resistant to the suppressive effects of ethanol in
the developing brain of ethanol-treated embryos. The overall increase
in GLUT-1 may reflect a deregulation of the transporter induced by
ethanol exposure. The increased IM localization and decreased amount of
PM GLUT-1 may be a mechanism used by the ethanol-treated cell to
maintain normal glucose uptake despite the overall increased level of
the transporter.
GLUT-3; fetal development; fetal alcohol syndrome; glucose uptake; chicken
