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Molecular mediators of metabolic processes, to increase energy expenditure, have become a focus for therapies of obesity. The discovery of cytokines secreted from the skeletal muscle (SKM), termed “myokines,” has garnered attention due to their positive effects on metabolic processes. Interleukin-15 (IL-15) is a myokine that has numerous positive metabolic effects and is linked to the PPAR family of mitochondrial regulators. Here, we aimed to determine the importance of PPAR α  and/or PPAR δ  as targets of IL-15 signaling. C2C12 SKM cells were differentiated for 6 days and treated every other day with IL-15 (100 ng/mL), a PPAR α  inhibitor (GW-6471), a PPAR δ  inhibitor (GSK-3787), or both IL-15 and the inhibitors. IL-15 increased mitochondrial activity and induced PPAR α , PPAR δ , PGC1 α , PGC1 β , UCP2, and Nrf1 expression. There was no effect of inhibiting PPAR α , in combination with IL-15, on the aforementioned mRNA levels except for PGC1 β  and Nrf1. However, with PPAR δ  inhibition, IL-15 failed to induce the expression levels of PGC1 α , PGC1 β , UCP2, and Nrf1. Further, inhibition of PPAR δ  abolished IL-15 induced increases in citrate synthase activity, ATP production, and overall mitochondrial activity. IL-15 had no effects on mitochondrial biogenesis. Our data indicates that PPAR δ  activity is required for the beneficial metabolic effects of IL-15 signaling in SKM.

IL-15 Mediates Mitochondrial Activity through a PPARδ-Dependent-PPARα-Independent Mechanism in Skeletal Muscle Cells