Henry Ford Hospital Medical Journal


Growth hormone (GH) synthesis and release is controlled by hypothalamic GH releasing factor. Thyroid hormones, androgens and estrogens in physiologic concentrations enhance GH secretion but a controlling role for glucagon and vasopressin in GH release is not established. Under stress, ACTH directly facilitates GH release while the similar action of the catecholamines is mediated by the a-adrenergic receptors. Though physiologic doses of glucorticoids and progestins do not affect GH liberation, prolonged administration of medroxyprogesterone acetate or of glucocorticoids in high dosage will decrease blood levels or blunt Gti responsiveness. GH enhances the release of insulin. A shift in adrenal steroid biosynthesis from the glucocorticoid to the androgenic pathway may also be an effect of GH administration. Prolonged elevated GH levels decrease serum thyroid binding globulin but increase the turnover of free thyroxine. Decreased thyroidal iodine uptake is probably secondary to these changes in thyroxine metabolism. In hypothyroidism and severe Cushing's syndrome GH release is blunted. In most cases of acromegaly as well as in hyperthyroidism GH is nonsuppressible, while in diabetes its response to stimuli other than hypoglycemia is exaggerated.



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