Possible role of somatostatin in the regulation of the sexually differentiated steroid metabolism and prolactin receptor in rat liver.

The regulation of the sexually differentiated metabolism of 4-[4-14C]androstene-3,17-dione and the presence of PRL receptors in rat liver were studied. Electrolytic lesions in male rats placed in a restricted area in the anterior hypothalamic periventricular area caused a feminization of hepatic steroid metabolism (i.e. increased the 5 alpha-reductase and decreased the 6 beta- and 16 alpha-hydroxylase activities) and of the levels of PRL receptors (increased binding of [125I]-labeled human PRL). After periventricular lesions, histochemical analysis revealed a decrease in somatostatin-like immunoreactive cell bodies in the periventricular area. Also the number of immunoreactive somatostatin fibers in the median eminence was dramatically reduced. Somatostatin levels in the median eminence, as measured by RIA, were reduced to approximately 2-10% of control values after periventricular lesions. Large lesions in the amygdaloid complex in male rats caused a partial feminization of hepatic steroid metabolism and PRL receptors. Passive immunization during 4 days by multiple injections of an antiserum generated against somatostatin resulted in a partial feminization of the male rat liver. When somatostatin was injected into female rats, the PRL receptors were reduced to approximately 60% of the control female receptor levels. The present study indicates that the anterior periventricular hypothalamic area is important in the control of the sexually differentiated steroid metabolism and PRL receptors in the liver and that the amygdaloid complex also may have regulatory influences on this system. A possible central neuro-endocrine mediator of these sex differences in the liver could be somatostatin or a related compound.