Chronic ethanol feeding in a high-fat diet decreases insulin
-stimulated glucose transport in rat adipocytes.
Wilkes, Jason J., Lorraine L. Deforrest, and Laura E. Nagy.
Department of Human Biology and Nutritional Sciencesm University of
Guelph, Guelph, Ontario N1G 2W1, Canada
APStracts 3:0100E, 1996.
Ethanol consumption has been associated with glucose intolerance and
insulin resistance and is suggested to be an independent risk factor
in the development of non-insulin dependent diabetes mellitus. We
have investigated the long term effects of ethanol consumption on
insulin regulated glucose transport in rat adipocytes. Male Wistar
rats were fed a high-fat liquid diet containing 35% ethanol (ethanol
-fed) or a control diet which isocalorically substituted maltose
dextrin for ethanol (ad lib). A third group was pair-fed control
diet. Basal rates of 2-deoxyglucose uptake were similar in adipocytes
from all three groups. Treatment with insulin increased 2
-deoxyglucose uptake in ad lib and pair-fed rats, but did not
stimulate uptake in ethanol-fed rats. Similarly, while okadaic acid
increased 2-deoxyglucose uptake in pair-fed rats, it had no effect in
ethanol-fed rats. GLUT1 quantity was greater in pair-fed and ethanol
-fed rats compared to ad lib controls. GLUT4 was decreased in ethanol
-fed rats compared to pair-fed, but not different from ad lib
controls. In ad lib and pair-fed rats, insulin increased the
translocation of GLUT4 to the cell surface by 2.0-fold. In contrast,
translocation of GLUT4 was not observed after insulin stimulation of
ethanol-fed rats, paralleling the loss of insulin stimulated glucose
uptake. In ethanol-fed rats, GLUT4 protein quantity was negatively
associated with increased Gas protein and isoproterenol stimulated
cAMP production. These data suggest that loss of insulin-stimulated
glucose uptake in rat adipocytes after chronic ethanol feeding is at
least partially due to decreased movement of GLUT4 to the cell
surface after insulin stimulation.
Received 19 January 1996; accepted in final form 6 May 1996.
APS Manuscript Number E30-6.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 28 May 96