PRRT2 and Insulin resistance: A large body of evidence supports the contention that insufficient mitochondrial capacity in skeletal muscle can trigger a buildup of lipid-derived molecules, including diacylglycerols and ceramides, that subsequently trigger activation of PKCθ, inhibitory serine phosphorylation of IRS1, and insulin resistance (Morino et al., 2006; Erion and Shulman, 2010).