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). This evidence concerns the gene FAM3A and Other metabolic disease.