Rac1 Regulates Contraction-Induced Glucose Uptake in Skeletal Muscle

摘要

In this issue of Diabetes(p. 1139), Sylow et al. establish that Ras-related C3 botulinum toxin substrate 1 (Rac1) is not only activated by muscle contraction but that it is also necessary for contraction-induced skeletal muscle glucose uptake. By quantifying the GTP-bound Rac1 immediately after exercise, the investigators demonstrated that Rad is activated by exercise in both mice and humans. Confirmatory experiments in mice showed Rac1 to be essential in contraction-induced glucose uptake. Soleus and extensor digitorum longus (EDL) muscles were incubated with one of two Rad inhibitors, NSC23766 or Rad inhibitor II. Treatment with either inhibitor decreased contraction-induced glucose uptake in the muscle. Treatment with NSC23766 reduced glucose uptake by -55% in both soleus and EDL muscle, and the corresponding decreases after treatment with Rad inhibitor II were 58% in soleus muscle and 22% in EDL.