We found that (i) FAM3A increased lipogenesis and the lipid content in muscles; (ii) FAM3A increased adiponectin levels and a positive correlation was observed between FAM3A and adiponectin levels in patient plasma samples; (iii) FAM3A inhibited IR and metabolic disorders; and (iv) these functions of FAM3A were due to the induction of PPARα expression and depended on the insulin receptor (insR). The gene discussed is PPARA; the disease is Other metabolic disease.