Moreover, as predicted by previous studies of transgenic mice expressing a constitutively active Akt construct specifically in skeletal muscle [8], the ursolic acid-mediated increase in skeletal muscle Akt activity was associated with skeletal muscle hypertrophy, increased energy expenditure, and reduced total body weight, white fat, glucose intolerance and hepatic steatosis. The gene discussed is AKT1; the disease is Hepatic steatosis.