Specific deletion of insulin receptors (IR) and leptin receptors (LepR) from the pro-opiomelanocortin (POMC) neurons in a mouse model (IR/LepRPOMC) results in a PCOS phenotype with female mice displaying irregular cycles, dysfunctional ovulation, reduced fertility, elevated circulating T and insulin levels, increased fat mass and adipocyte hypertrophy, as well as reduced glucose tolerance and insulin resistance (140, 141). The gene discussed is INS; the disease is polycystic ovary syndrome.