In vivo chorionic gonadotropin administration reverses the testosterone secretory defect of Leydig cells from old rats.
Old male rats have decreased serum testosterone, luteinizing hormone (LH), follicle -stimulating hormone (FSH), Leydig cell testosterone secretory responsiveness to chorionic gonadotropin (hCG), and gonadotropin binding capacity. Although prolonged in vivo hCG administration restores serum testosterone, in vitro hCG exposure of Leydig cells does not reverse their age-related hyporesponsiveness. To explore this discrepancy, we studied Leydig cell function before and after hCG administration in vivo (treatment). Before treatment, old rats had lower serum testosterone, in vitro testosterone and cyclic adenosine monophosphate (cAMP) production, both basally and in response to hCG, and reduced hCG binding capacity. After treatment, old and young rats did not differ in any of these parameters. hCG binding and cAMP responses were reduced in both old and young rats. Thus, prolonged in vivo exposure to hCG appeared to reverse both the in vivo and in vitro age-related Leydig cell secretory defect, despite gonadotropin receptor down-regulation. This suggests that the "aging" defect(s) are caused by chronic gonadotropin deprivation.
D000375:Aging; D000818:Animals; D006063:Chorionic Gonadotropin / Q000378:metabolism*; D000242:Cyclic AMP / Q000378:metabolism; D007985:Leydig Cells / Q000378:metabolism*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D013739:Testosterone / Q000378:metabolism*
D006063:Chorionic Gonadotropin; D013739:Testosterone; D000242:Cyclic AMP