Effects of Ethanol on Carbohydrate Metabolism in the Elderly

We have previously reported that in young men, ethanol caused acute insulin resistance, but compensatory insulin secretion prevented deterioration of glucose tolerance (1). In this study, we tested the hypothesis that elderly men, because of their pre-existing insulin resistance and compromised insulin secretory capacity, may experience worsening of their glucose tolerance after ethanol. Nine elderly men (65.7 ± 0.8 yr, BMI 25.8 ± 1.4 kg/m2) received ethanol (13 mmol/kg for 30 min i.v.) or saline followed 30 min later by i.v. glucose (2.8 mmol/kg for 5 min). To determine the mechanism of the ethanol effect, six of the men underwent euglycemic-hyperinsulinemic (∼350 pM) clamping with simultaneous infusion of ethanol or saline. Muscle biopsies were obtained before and 1 and 4 h after insulin infusion. In all nine men, glucose concentrations after i.v. glucose were higher after ethanol than after saline, whereas insulin was the same and glucose tolerance decreased by 23% (Kg 2.41 ± 0.2 vs. 1.86 ± 0.1%/min, P < 0.01). Ethanol reduced insulin-stimulated glucose uptake from 40.6 ± 3.1 to 25.6 ±1.9 μmo; · kg−1 · min−1 (−37%, P < 0.05), glucose oxidation from 11.7 ± 1.1 to 7.0 ±0.7 μmol · kg−1 · min−1 (−33%, P < 0.01), and glucose storage from 28.7 ± 2.4 to 18.6 ±1.7 μmol · kg−1 · min−1(−35%, P <0.01). Ethanol increased muscle lactate concentration from 0.49 ± 0.14 to 1.99 ± 0.99 μmol/mg protein (P < 0.05), but had no effects on muscle concentration of freeglucose, G-6-P, and citrate concentrations, nor did it affect muscle GS activity. We concluded that modest amounts of ethanol in elderly men impaired glucose oxidation and caused insulin resistance, which because of lack of compensatory insulin secretion, resulted in deterioration of glucose tolerance.