Excess androgen in early gestation programs both hyperinsulinemia from adiposity-dependent insulin resistance and preferential accumulation of visceral adiposity, whereas androgen excess later in gestation decreases insulin sensitivity and increases non-visceral abdominal fat, although insulin secretion is unaffected (Bruns et al. 2007, Abbott et al. 2010). The gene discussed is INS; the disease is hyperinsulinism.