Alcohol consumption improves insulin signaling in the myocardium

In a previous study, we demonstrated that swine with metabolic syndrome treated with alcohol had improved insulin signaling. We developed a follow-up study to evaluate the effects of alcohol on ischemic myocardium in animals without metabolic syndrome.

Fourteen Yorkshire swine underwent placement of an ameroid constrictor to induce chronic myocardial ischemia. Postoperatively, one group was supplemented with ethanol (ETOH), and one group was supplemented with sucrose (SUC) daily to normalize caloric intake. After 7 weeks, all animals underwent dextrose challenge and harvest of nonischemic and ischemic myocardium. Tissues were analyzed for protein expression and histologic analysis.

There was no difference in body mass index, serum glucose or insulin levels. However, ethanol supplementation up-regulated phosphoinostitide 3-kinase, phosphorylated protein kinase B, protein kinase B, and phosphorylated Forkhead Box 01 expression, which may promote insulin signaling, and down-regulated inhibitors of insulin signaling pIRS1 and pIRS2. There was no difference in intramyocardial glycogen but there was increased GLUT4 expression in the ETOH group, which may promote glucose use.

Despite similar serum glucose and insulin levels, alcohol consumption up-regulates the insulin signaling pathway in the absence of metabolic syndrome in both nonischemic and chronically ischemic myocardium. These results suggest that alcohol selectively up-regulates the insulin signaling pathway despite normoglycemia.