Disorders of the adrenal cortex and medulla can result in glucose intolerance or overt diabetes mellitus. Cushing's syndrome, characterized by excessive secretion of glucocorticoids, impairs glucose tolerance primarily by causing insulin resistance at the post-receptor level. On the other hand, phaeochromocytoma and hyperaldosteronism, via the respective actions of catecholamines and hypokalaemia on the pancreatic beta-cell, impair glucose tolerance primarily by inhibiting insulin release. The glucose intolerance associated with these adrenal disorders is usually only mild to moderate in severity. Marked hyperglycaemia, glycosuria, and polyuria are uncommon and ketosis is rare. Moreover, the late complications of diabetes mellitus are distinctly uncommon in patients with these disorders, and the prognosis for morbidity and death is usually that of the underlying disease and not that of diabetes mellitus. The impaired glucose tolerance induced by all three of these adrenal disorders usually returns to normal once the underlying aetiology has been cured. These factors must guide the clinician in treatment of these secondary forms of diabetes, and suggest that tight (near normal) blood glucose control may not be an appropriate goal in patients with these disorders. The relationship between adrenal androgens and glucose tolerance is more uncertain. Several studies in humans have demonstrated an acute decline in serum concentrations of the adrenal steroids DHEA and DHEA-sulfate in response to experimentally-induced hyperinsulinaemia, but the regulatory role of insulin on adrenal androgen metabolism in normal physiology or disease remains speculative. In several animal models DHEA appears to exert potent anti-obesity and anti-diabetogenic actions, but such effects have yet to be demonstrated in humans. Human studies of DHEA are limited, and more research needs to be conducted to determine whether the observations made in animal models will prove applicable to man.