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

• Published in: Interventional medicine and applied science 2018-12, Vol.10 (4), p.226-232
• Main Authors: de França, Igor Rabelo, Meneses-Santos, Daniela, Moreira, Gabriela Virginia, Lima, Fábio Bessa, Carvalho, Carla Roberta de Oliveira, Marçal, Anderson Carlos
• Format: Article
• Language: English
• Subjects: Cellular signal transduction; Dexamethasone; Diabetes mellitus; Dosage and administration; Drug therapy; Facial muscles; Health aspects; Insulin; Original Paper; Physiological aspects
• ISSN: 2061-1617; 2061-5094
• DOI: 10.1556/1646.10.2018.44

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. 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. 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. The degree of phosphorylation/activity in the masseter muscle is different from that in other muscle territories.