Type 2 diabetes is the most common form of hyperglycemia. The disease exists in all populations, but in developed societies, the prevalence has risen as the population ages and above all becomes more obese. In the prediabetic state, type 2 diabetes involves two defects, peripheral insulin resistance and hyperinsulinemia, which is followed by the failure of insulin secretion to compensate for the insulin resistance. As with nearly any disease, it is likely that multiple environmental and genetic factors are involved in the development of insulin resistance. An acquired pathogenic factor is obesity, particularly visceral obesity. Compelling evidence suggests that progressive dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis, with elevated levels of circulating cortisol, is implicated in the development of visceral obesity. The HPA axis perturbations associated with visceral obesity can be accounted for, in part, by increased environmental stress that destabilizes the hypothalamic-pituitary system in individuals with genetic susceptibility.