Insulin signaling pathway in the masseter muscle of dexamethasone-treated rats.

BACKGROUND AND AIMS: The treatment with glucocorticoids may induce molecular changes in the level and/or degree of phosphorylation of proteins located downstream of the insulin receptor/insulin-like growth factor receptor (IR/IGF1R) in many tissues. However, few studies have investigated the intracellular insulin pathway in the masseter muscle. Therefore, this study aimed to analyze the IR/IGF1R signaling pathway in the masseter muscle of rats treated with dexamethasone. MATERIALS AND METHODS: Male Wistar rats were divided into two groups: control group (intraperitoneally injected with 0.9% NaCl solution) and dexamethasone group [intraperitoneally injected with 1 mg/kg (bw) dexamethasone solution] for 10 consecutive days. Sections of the masseter muscle were removed at time zero and after the infusion of regular insulin into the portal vein. RESULTS: Dexamethasone administration induces body weight loss without changing masseter muscle weight and reduces the expression of total IR and PI3K proteins; total levels of IRS1, Akt, and ERK1 remain unchanged between groups. The degree of phosphorylation/activity of IRS1 after insulin stimulus increased only in the control group; degree of phosphorylation of Akt increased in both groups, but this increase was attenuated in the dexamethasone group. DISCUSSION AND CONCLUSION: The degree of phosphorylation/activity in the masseter muscle is different from that in other muscle territories.