Although pituitary gonadotropins are the major regulators of gonad function in vertebrates, an increasing number of reports indicate that growth hormone (GH) could act on ovarian and testicular function (for reviews, see ). Pubertal development that has been delayed in isolated GH deficiency in both humans and animals can be restored by GH treatment . The first step in GH action is binding to specific receptors on the cell surface of the target tissue. Low levels of GH receptor (GH-R)/GH-binding protein (GH-BP) mRNA have been described in testis in the chicken , the rat , the rabbit , and human. ventolin inhalers
Lobie et al. , using an immunohistochemistry approach, found intense GH-R/GH-BP immunoreactivity in the male reproductive system, including numerous testicular cell types. Although a direct action of GH at the gonadal level has been proposed, the mechanisms by which GH exerts its action are unclear and poorly documented in the testis. In hypophysectomized male rats, exogenous GH administration improved testicular steroidogenic response to LH and LH receptor content and increased insulin-like growth factor (IGF)-I mRNA content and IGF-I peptide accumulation in the testis. Furthermore, GH stimulation of IGF-I mRNA content in Leydig/interstitial cell culture and IGF-I peptide accumulation in Sertoli cell culture have also been reported. These results suggest that IGF-I might be an important modulator/mediator of GH action in the testis.