Glucose Metabolism And MHC Isoforms Expression In Skeletal Muscle In Leptin Transgenic Skinny Mice

Abstract

Leptin is an adipocyte-derived hormone and may play an important role in the regulation of energy homeostasis. Previous studies have suggested that the overexpression of leptin activates AMPK in skeletal muscles to increase glucose and lipid metabolism. PURPOSE To determine whether the overexpression of leptin can change myosin heavy chain (MHC) isoforms coordinatedly with the metabolic enzyme activities. METHODS Male leptin transgenic mice (n=5, Tg) and the control (n=7, Cont) were used. The composition of MHC isoforms (type I, typeIIa/x and type IIb) of gascrocnemius (Gas), tibialis anterior (TA), plantaris (Pl), extensor digitorum longus (EDL), and soleus muscles (Sol) were determined by SDS-PAGE. Citrate synthase (CS), hydroxyacyl-CoA dehydrogenase (HAD) and lactate dehydrogenase (LDH) activities of the deep portion of the TA muscles were also measured. RESULTS There were no significant differences in MHC isoforms expression in any muscles between Tg and Cont, but in the average type IIb MHC to type IIa/x shift was observed. The ratio of CS to LDH activity was significantly higher in Tg group than in Cont (0.262 vs. 0.224, p < 0.013), though there were no significant difference in the CS, HAD and LDH activities between groups (p > 0.05). CONCLUSIONS From these data we concluded that the overexpression of leptin increased glucose metabolism more aerobically, whereas the MHC composition did not change.