Effect of M35, a neuropeptide galanin antagonist on glucose uptake translated by glucose transporter 4 in trained rat skeletal muscle

Abstract

In this study, we used M35, a galanin antagonist to explore the effect of an increase in galanin release induced by exercise on glucose transporter 4 (GLUT4) content and function. The rats tested were divided into four groups: rats from sedentary and trained drug groups were injected by M35, 5 times per week during four weeks. Rats from sedentary and trained control groups by 0.1 mol/l citrate buffer. The rats from both exercise groups swam after each injection. The results showed that M35 significantly decreased glucose infusing speeds in euglycemic–hyperinsulinemic clamp tests. M35 treatment elevated plasma insulin levels in both drug groups. And the insulin levels in both drug groups were higher also than that after experiments in each control group respectively. The four weeks swimming enhanced the plasma galanin contents. The galanin levels after experiments in both exercise groups were higher than that in each sedentary control group respectively too. The GLUT4 densities were attenuated by M35 at plasma membranes and total cell membranes. The change ratios of GLUT4 immunoreaction at plasma membranes to total cell membranes were lower in both drug groups compared to each control group. Those results suggest that endogenous galanin has an important attribute to elevate the insulin sensitivity by increasing GLUT4 contents and promoting GLUT4 transportation from intracellular membranes to plasma membranes in muscle cells. Galanin is an important hormone to elevate insulin sensitivity in rest and exercise conditions.