Alcohol intake impairs glucose counterregulation during acute insulin-induced hypoglycemia in IDDM patients. Evidence for a critical role of free fatty acids.

In this study, we assessed the effects of alcohol intake on glucose counterregulation in response to acute insulin-induced hypoglycemia in IDDM patients and in normal control subjects. Nine euglycemic IDDM patients and 9 normal control subjects were studied. After a baseline period, insulin (0.15 U/kg) was administered subcutaneously to induce hypoglycemia. Each IDDM patient was studied 3 times. In the first study, alcohol was orally administered as wine. In the second (control) study, water was administered instead of wine. In the third study, wine was given; however, a continuous infusion of heparin plus intralipid was administered to prevent the fall in plasma free fatty acid. Normal control subjects underwent only the alcohol and the control studies. In IDDM patients alcohol intake impairs, whereas in normal subjects it supports glucose counterregulation. Alcohol intake is associated with normal catecholamine responses in both IDDM diabetic patients and normal subjects. In both IDDM patients and normal subjects, hepatic glucose production in the recovery phase of the alcohol study was normal. Plasma glucose rate of disappearance was significantly increased by alcohol intake in IDDM (13.72 +/- 0.82 vs. 11.84 +/- 0.53 mumol.kg-1 x min-1; P < 0.05). Alcohol intake in both normal subjects and IDDM patients decreased plasma free fatty acid (267 +/- 22 vs. 156 +/- 20 microM; P < 0.01 and 356 +/- 29 vs. 96 +/- 12 microM; P < 0.01). We hypothesized that in IDDM patients, deficient glucose recovery during alcohol intake is the result of the ability of alcohol to depress lipolysis.