CHRONIC ETHANOL FEEDING IMPAIRS GLUCOSE-TOLERANCE BUT DOES NOT PRODUCE SKELETAL-MUSCLE INSULIN-RESISTANCE IN RAT EPITROCHLEARIS MUSCLE

Herein, we have investigated whether male Wistar rats develop impaired glucose tolerance after ethanol feeding, Rats were fed a liquid diet providing 35% calories from ethanol (EF) or a control diet that isocal orically replaced ethanol with maltose-dextrins for 4 weeks, Intraveno us glucose tolerance was impaired in EF rats compared with pair-fed (P F), but not ad libitum (AL) controls, Areas under the intravenous gluc ose tolerance test curve were 5476 +/- 516 mm(2), 3056 +/- 421 mm(2), and 4199 +/- 613 mm(2) (p < 0.05) for AL, PF, and EF rats, respectivel y, Initial plasma insulin concentrations in EF rats were comparable wi th PF rats; however, 15 min after a dextrose challenge, plasma insulin levels in EF rats were 39% lower than PF mts, Because skeletal muscle is the primary sink for insulin-mediated glucose disposal, the develo pment of skeletal muscle insulin resistance after ethanol feeding coul d contribute to impaired glucose tolerance. Total GLUT1 was not affect ed by diet in either red or white muscle. No difference in the total q uantity of insulin-responsive glucose transporter, GLUT4, was observed in red muscle, In contrast, GLUT4 was 20% lower in white muscle from EF rats, compared with PF and AL rats. However, insulin-stimulated glu cose transport into the epitrochlearis, a white muscle group, was not impaired with ethanol feeding. These data demonstrate that chronic eth anol feeding impairs glucose tolerance; impaired glucose tolerance was associated with an inability to maintain plasma insulin levels, rathe r than the development of skeletal muscle insulin resistance.