Leptin inhibits glycogen synthesis in the isolated soleus muscle of obese (ob/ob) mice

Abstract

The ob gene product, leptin, causes significant and dose-dependent inhibition of basal and insulin-stimulated glycogen synthesis in isolated soleus muscle from ob/ob mice, and a smaller, non-significant inhibition in muscle from wild-type mice. Leptin had no inhibitory effect on glycogen synthesis in soleus muscle from the diabetic (db/db) mice, which lack the functional leptin receptor. The full-length leptin receptor (Ob-Rb), is expressed in soleus muscle of both ob/ob and wild-type mice, however with no detectable differences in expression level. These results suggest that hyperleptinaemia may attenuate insulin action on glucose storage in skeletal muscle.