title: Differential effects of follicle-stimulating hormone and luteinizing hormone on Leydig cell function and restoration of spermatogenesis in hypophysectomized and photoinhibited Djungarian hamsters (Phodopus sungorus).
abstract: Effects of pure human follicle-stimulating hormone (hFSH) and ovine luteinizing hormone (oLH) on testicular function were investigated in long-term hypophysectomized or photoinhibited Djungarian hamsters. hFSH (5 IU) or oLH (5 micrograms) or a combination of FSH and LH (5 IU and 5 micrograms, respectively) were injected s.c. twice daily for 7 days to hypophysectomized and photoinhibited hamsters. Other photoinhibited hamsters were treated for 14 and 21 days with FSH and LH (3 IU and 3 micrograms, respectively) in a similar way. LH alone had little, if any, effect on testicular weights; FSH, when injected alone or in combination with LH (FSH/LH), caused a significant increase in testes weights at each time point. On the other hand, LH or FSH/LH, but not FSH alone, caused a significant increase in the accessory organ weights. FSH had no effect on intratesticular testosterone (T) or on 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) activity but enhanced the in vitro response of interstitial cells to hCG. LH and FSH/LH had pronounced effects on intratesticular T, 3 beta-HSD activity, and in vitro response of interstitial cells to human chorionic gonadotropin. Treatment with FSH or FSH/LH caused regrowth of the testis and restoration of tubular lumen and tubular diameter and restored complete spermatogenesis. However, LH had little effect on spermatogenesis in spite of increased intratesticular and peripheral T levels. These results indicate that although LH can cause a full redifferentiation of Leydig cells in photoinhibited hamsters, it has only minor effects on tubular function. On the other hand, FSH alone induces full restoration of tubular function in these animals and has no direct effect on Leydig cell steroidogenesis, but may enhance the Leydig cell responsiveness to LH.
authors.affiliation: Max Planck Clinical Research Unit for Reproductive Medicine, Institute of Reproductive Medicine, Münster, Federal Republic of Germany.
authors.forename: P
authors.initials: P
authors.lastname: Niklowitz
authors.forename: S
authors.initials: S
authors.lastname: Khan
authors.forename: M
authors.initials: M
authors.lastname: Bergmann
authors.forename: K
authors.initials: K
authors.lastname: Hoffmann
authors.forename: E
authors.initials: E
authors.lastname: Nieschlag
mesh_terms: D015096:3-Hydroxysteroid Dehydrogenases / Q000378:metabolism; D000818:Animals; D006063:Chorionic Gonadotropin / Q000494:pharmacology; D006224:Cricetinae; D005640:Follicle Stimulating Hormone / Q000494:pharmacology*; D005837:Genitalia, Male / Q000033:anatomy & histology; D007016:Hypophysectomy; D007985:Leydig Cells / Q000187:drug effects / Q000502:physiology*; D008027:Light; D007986:Luteinizing Hormone / Q000494:pharmacology*; D008297:Male; D009929:Organ Size; D013091:Spermatogenesis / Q000187:drug effects* / Q000502:physiology; D013737:Testis / Q000032:analysis / Q000033:anatomy & histology / Q000378:metabolism; D013739:Testosterone / Q000032:analysis / Q000378:metabolism
chemical_list: D006063:Chorionic Gonadotropin; D013739:Testosterone; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D015096:3-Hydroxysteroid Dehydrogenases