Regulation of sexually dimorphic hepatic steroid metabolism by the somatostatin-growth hormone axis.

Lesions in the periventricular hypothalamic area in male rats results in a "feminization" of steroid metabolizing enzymes in the liver. These lesions also resulted in a decrease of somatostatin levels in the median eminence. Since blockade of somatostatin by in vivo administration of an antiserum also caused "feminization" of the liver, it is possible that at least one hypothalmic factor responsible for "feminization" is related to somatostatin. Also extrahypothalmic areas seem to influence sexually differentiated functions in the liver. The neuroendocrine control of the "feminizing factor" secretion from the pituitary bears several resemblances to the central control of GH. The hypothesis that the plasma pattern of GH regulates hepatic steroid metabolism in the rat was studied in two different animal models: (1) Different plasma patterns of GH were achieved by administration of human GH (hGH) at different frequencies or by infusing the hormone continuously by means of Alzet osmotic minipumps to hypophysectomized female rats. (2) The plasma pattern of GH in animals with an intact pituitary gland was investigated under conditions which lead to "feminization" of hepatic steroid metabolism. The results demonstrate that the plasma pattern of GH influences hepatic steroid metabolism. Increased trough plasma GH values or absence of time periods with undetectable plasma levels of GH appears to be a major determinant for "feminization" of hepatic steroid metabolism. Since sex steroids were found to influence the plasma pattern of GH it seems as if differences in the plasma pattern of GH between male and female rats explain the sex-differentiated hepatic steroid metabolism.