Obesity is associated with different disturbances in endocrine function. Both spontaneous growth hormone (GH) secretion and its response to several stimuli have shown to be reduced in obese patients. The GH responses to GH-releasing hormone and other challenges by pyridostigmine suggest that the reduction in GH secretion is related to an increased somatostatinergic tone. Other experiments point to a down-regulation of somatostatin receptors in the somatotroph cell. Ghrelin administration is followed by a massive GH release, but the possibility that ghrelin or GHRH deficiency are the cause of GH deficiency in obesity is unlikely. The increase in free fatty acids in obesity might be related to GH reduction, since acipimox administration is able to reverse GH secretion. In women, abdominal obesity is associated with hyperandrogenism and low sex hormone-binding globulin levels. Obese men have low testosterone and gonadotrophin concentrations, specially in cases of morbid obesity. An increase in hypothalamic-pituitary-adrenal axis activity and some resistance to dexamethasone suppression have been described in abdominal obesity. This effect may be due to neuroendocrine alterations related to a genetic origin. Adrenal hyperfunction may favour cardiovascular and metabolic complications. There are no disturbances in thyroid function. Sometimes a reduction in prolactin response to several stimuli has been reported. This effect may be due to hyperinsulinaemia or to disturbances in the dopaminergic tone.