PTG gene deletion causes impaired glycogen synthesis and developmental insulin resistance
J. Clin. Invest. Sean M. Crosson, et al. 111:1423 doi:10.1172/JCI17975 [Go to this article.]

Figure 7
Skeletal muscle of 18-month-old PTG+/– mice displays increased triglyceride content and inhibition of insulin signaling pathways involved in glucose transport and glycogen synthesis. (a) Skeletal muscle triglyceride content is increased in 18-month-old PTG+/– mice. Skeletal muscle triglyceride content was estimated from organic solvent–extracted epitrochlearis muscle isolated from fasting 18-month-old animals (n = 4–12 per group). Results are reported as mean ± SEM (*P ≤ 0.05). (b) Insulin signaling is affected in the skeletal muscle of aged PTG+/– mice. Protein lysates were prepared from muscle of 9- to 10-month-old nonfasting male animals either in the basal state or after injection with 2 mU/g body weight human recombinant insulin. Western blotting was performed for total and phosphospecific Akt. Muscle homogenates were immunoprecipitated with an antibody against IRS-1 and immunoblotting was performed to determine the levels of total IRS-1 and tyrosine-phosphorylated IRS-1.