Glucocorticoids and neuroendocrine function

Recent experimental evidence supports the role of glucocorticoids in the ne uroendocrine control of food intake and energy expenditure. In particular, glucocorticoids promote food consumption directly through stimulation of NP Y and inhibition of CRH and melanocortin release. CRH and NPY are also func tionally linked by a mutual regulation. CRH is anorexigenic when secreted a cutely while it exerts the opposite effect when, upon sustained secretion, it stimulates the hypothalamo-pituitary-adrenal (HPA) axis. The orexigenic effects of glucocorticoids are counteracted by a steroid-induced rise in le ptin levels that closes a regulatory loop regarding food consumption. Furth ermore, glucocorticoids may alter body fat distribution, increasing truncal adiposity both directly and by inhibition of growth hormone secretion. No clearcut alterations of the HPA function are apparent in obesity as a whole . However, subtle and specific abnormalities may be noted in subsets of obe se patients. Indeed, obesity, mostly visceral type, is associated with an i ncreased cortisol clearance and 11-beta hydroxysteroid dehydrogenase activi ty in the omental fat. In the same vein, an increased cortisol rise followi ng a mixed meal has been observed in obese subjects. Finally, it has been p roposed that adrenal incidentalomas, often characterized by enhanced cortis ol secretion, might be a clinical expression of the X syndrome.