Postnatal inhibition of myostatin signaling in mice with diet-induced obesity will be necessary to directly compare these two muscle hypertrophy models to determine whether the reduction in adipose tissue mass in HFD-fed constitutively active Akt1 mice is caused by hypertrophy of fast glycolytic fibers, by increasing the activation of the Akt signaling pathways, or both. Here, MSTN is linked to obesity disorder.