Excess delivery of PA to skeletal muscle is implicated in the development of insulin resistance resulting from lipid oversupply to skeletal muscle [3,4,5], inhibitory effects on the insulin signaling, mediated by Protein kinase C theta-dependent activation of mammalian target of rapamycin (mTOR)/p70 ribosomal S6 kinase (S6K) pathway [6] and loss of muscle mass [7,8,9]. This evidence concerns the gene MTOR and Insulin resistance.