Moreover, the present findings are also consistent with observations reported by Cotero et al23 of an increased sensitivity of cultured VMH GE neurons isolated from insulin‐resistant versus insulin‐sensitive rats to the inhibitory effects of local hypoglycaemia on their activity, an alteration that would potentiate a CRR at euglycaemic levels facilitating hyperglycaemia and glucose intolerance (ie when insulin resistance is present, GE neurons stop firing earlier as glucose levels decline in the postabsorptive state). The gene discussed is INS; the disease is Hyperglycemia.