Chemerin reduced insulin-stimulated Akt1 phosphorylation and activation of 5’AMP-activated protein kinase (AMPK) in the skeletal muscle and induced insulin resistance in skeletal muscle. Overexpression of chemerin in mice decreased skeletal muscle mitochondrial content and increased mitochondrial autophagy. Chemerin treatment of C2C12 myotubes increased the production of mitochondrial reactive oxygen species. The gene discussed is AKT1; the disease is Insulin resistance.