IL-6 Induces an Increase in Insulin Sensitivity of Glucose Transport

Abstract

PURPOSE An acute bout of exercise induces an increase in glucose transport in skeletal muscle. As the acute increase in glucose transport reverses immediately following exercise, a marked increase in insulin sensitivity occurs. Although this phenomenon was discovered more than 20 years ago, very little is known about the underlying mechanism. Recent results from our lab showed that activation of p38MAPK by anisomycin results in an increase in insulin sensitivity that is completely attenuated by the p38MAPK inhibitor, SB202190. IL-6 increases dramatically with exercise and has been shown to activate p38MAPK. Based on this information, we hypothesize that incubation with IL-6 will result in an increase in insulin sensitivity, possibly through a p38MAPK mediated pathway. METHODS To test this hypothesis, rat epitrochlearis muscles were incubated for 30 min in rat serum iwth IL-6 (120ng/ml). Glucose transport was measured 3.5 h after exposure to IL-6. Muscles were exposed to a submaximal insulin dose (60uU/ml) for 30 min before and during measurement of glucose transport. RESULTS Pre-incubation with IL-6 resulted in an increase in insulin-stimulated glucose transport ∼50% above that of control muscles. CONCLUSIONS The increase in insulin sensitivity of glucose transport with IL-6 is most likely mediated by activation of p38MAPK.