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The TGFβ family member myostatin (growth/differentiation factor-8) is a negative regulator of skeletal muscle growth. The hypermuscular Compac mice carry the 12-bp Mstn(Cmpt-dl1Abc) deletion in the sequence encoding the propeptide region of the precursor promyostatin, and additional modifier genes of the Compac genetic background contribute to determine the full expression of the phenotype. In this study, by using mice strains carrying mutant or wild-type myostatin alleles with the Compac genetic background and nonmutant myostatin with the wild-type background, we studied separately the effect of the Mstn(Cmpt-dl1Abc) mutation or the Compac genetic background on morphology, metabolism, and signaling. We show that both the Compac myostatin mutation and Compac genetic background account for determination of skeletal muscle size. Despite the increased musculature of Compac s, the absolute size of heart and kidney is not influenced by myostatin mutation; however, the Compac genetic background increases them. Both Compac myostatin and genetic background exhibit systemic metabolic effects. The Compac mutation decreases adiposity and improves whole body glucose uptake, insulin sensitivity, and 18 FDG uptake of skeletal muscle and white adipose tissue, whereas the Compac genetic background has the opposite effect. Importantly, the mutation does not prevent the formation of mature myostatin; however, a decrease in myostatin level was observed, leading to altered activation of Smad2, Smad1/5/8, and Akt, and an increased level of p-AS160, a Rab-GTPase-activating protein responsible for GLUT4 translocation. Based on our analysis, the Compac genetic background strengthens the effect of myostatin mutation on muscle mass, but those can compensate for each other when systemic metabolic effects are compared.

Myostatin propeptide mutation of the hypermuscularCompactmice decreases the formation of myostatin and improves insulin sensitivity