Abstract
Introduction Chronic resistance exercise induces improved hyperglycemia in patients with type 2 diabetes mellitus. Musclin, a muscle-derived secretory factor, is involved in the induction of insulin resistance via the downregulation of the glucose transporter-4 (GLUT-4) signaling pathway in skeletal muscles. However, whether musclin affects the mechanism of resistance exercise remains unclear. This study aimed to test the hypothesis that decreased muscle-derived musclin secretion in chronic resistance exercise is involved in improvement of insulin resistance via the GLUT-4 signaling pathway in rats with type 2 diabetes. Methods Male, 20-week-old, Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a type 2 diabetes model, were randomly divided into two groups: sedentary control (OLETF-Con) and chronic resistance exercise (OLETF-RT; climbing a ladder three times a week on alternate days for 8 weeks), whereas Long-Evans Tokushima Otsuka (LETO) rats were used as the nondiabetic sedentary control group. Results OLETF-Con rats showed increased fasting glucose levels, decreased insulin sensitivity index (QUICKI), muscle GLUT-4 translocation, and protein kinase B (Akt) phosphorylation, and concomitantly increased muscle musclin expression as compared with LETO rats (P < 0.01). In contrast, OLETF-RT rats significantly reduced muscle musclin expression, improved fasting glucose levels, and QUICKI through an accelerated muscle GLUT-4/Akt signaling pathway as compared with OLETF-Con rats (P < 0.01). Moreover, musclin protein levels in skeletal muscle were positively correlated with fasting blood glucose (r = 0.717, P < 0.01), and negatively correlated with QUICKI (r = -0.491, P < 0.05), muscle Akt phosphorylation (r = -0.475, P < 0.05), and GLUT-4 translocation levels (r = -0.643, P < 0.01). Conclusions These findings suggest that the reduction in muscle-derived musclin production by chronic resistance exercise may be involved in improved insulin resistance in rats with type 2 diabetes.
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