Impact of One-Week Administration of Dihydrotestosterone in Rat Anterior Pituitary Gland.

Hyperandrogenism causes dysfunction of the hypothalamic-pituitary-gonadal (HPG) axis in reproductive women. In this study, we examined the effects of dihydrotestosterone (DHT) on characteristic changes in rat anterior pituitary gland samples. DHT was administered to ovary-intact 6-week postnatal female rats for 7 days, after which the anterior pituitary glands were examined and compared with those in control rats. Estrous cyclicity was not drastically disrupted by DHT treatment. Common gonadotropin α subunit ( Cga ), luteinizing hormone β subunit ( Lhb ), and follicle-stimulating hormone (FSH) β subunit ( Fshb ) gene expression levels were not modulated by DHT treatment, while prolactin ( Prl ) gene expression was significantly repressed by DHT. Gonadotropin-releasing hormone (GnRH) receptor ( Gnrh-r ) gene expression was significantly inhibited by DHT, whereas pituitary adenylate cyclase-activating polypeptide (PACAP) receptor ( Pca1-r ) gene expression was increased by DHT. Gene expression levels of the receptors encoded by thyrotropin-releasing hormone ( Trh-r ) and kisspeptin ( Kiss1-r ) genes were unchanged. Expression of inhibin α subunit ( Inha ) and activin β A subunits ( Actba ) within the pituitary was inhibited by DHT treatment, while activin B subunit ( Actbb ) and follistatin ( Fst ) gene expression was unchanged by DHT. In mouse pituitary gonadotroph L β T2 cells, DHT did not modulate the gene expression of Gnrh-r , but it inhibited the expression of Inha and Actba subunits within the L β T2 cells. In rat prolactin-producing GH3 cells, DHT did not modulate prolactin gene expression, but it increased Pac1-r gene expression. The present observations suggest that DHT directly or indirectly affects the anterior pituitary gland and induces characteristic changes in hormone-producing cells.