Therefore, the aims of the present study was to determine which of the conditions of hyperinsulinemia and/or hyperandrogenism induce hepatic steatosis and inflammation in vivo and to what extent, if any, the resulting phenotype leads to the dysregulation of lipid metabolism, impairment in insulin-mediated IRS–PI3K–Akt signaling, and changes to inflammatory, apoptotic and autophagic responses as well as hepatocyte cell injury. The gene discussed is INS; the disease is hyperinsulinism.