title: [Endocrinological profile of human spermatogenic impairment--evaluation of function of Leydig and Sertoli cells in vivo or in vitro studies].
abstract: In vivo and in vitro studies were performed to determine the function of Leydig and Sertoli cells of the human testis with various degrees of spermatogenic impairment. The increases in basal and peak serum levels of luteinizing hormone (LH) and follicle stimulating hormone (FSH) after LH-RH administration correlated with the degree of impairment of spermatogenesis, and the basal peripheral blood levels of testosterone and that after human chorionic gonadotropin (hCG) administration for patients with moderate or severe impairment were significantly lower than the values for those with mild impairment. The concentration of testosterone in the internal spermatic vein of varicocele patients with or without hCG treatment did not differ between in mild and moderate impairment. In studies on cultured Sertoli cells, the production rate of plasminogen activator in patients with severe impairment was significantly lower than that in patients with moderate or mild impairment. The decrease in testicular high-affinity binding site for FSH correlated with the degree of hypospermatogenesis found in idiopathic male infertility, but, on the contrary, the hCG (LH) receptors showed no correlation with the degree of impairment of spermatogenesis. In the investigation of the relationship between testicular FSH receptors and the effectiveness of human menopausal gonadotropin (hMG)-hCG treatment on idiopathic male infertility, the presence or absence of testicular FSH receptors predicted the responsiveness to the treatment.
authors.affiliation: Department of Urology, Osaka University Hospital.
authors.forename: A
authors.initials: A
authors.lastname: Okuyama
authors.forename: N
authors.initials: N
authors.lastname: Nonomura
authors.forename: M
authors.initials: M
authors.lastname: Nakamura
authors.forename: M
authors.initials: M
authors.lastname: Namiki
authors.forename: M
authors.initials: M
authors.lastname: Matsuda
authors.forename: Y
authors.initials: Y
authors.lastname: Doi
authors.forename: T
authors.initials: T
authors.lastname: Matsui
authors.forename: E
authors.initials: E
authors.lastname: Koh
authors.forename: N
authors.initials: N
authors.lastname: Kondoh
authors.forename: M
authors.initials: M
authors.lastname: Takeyama
mesh_terms: D006063:Chorionic Gonadotropin; D005640:Follicle Stimulating Hormone / Q000097:blood*; D006801:Humans; D066298:In Vitro Techniques; D007248:Infertility, Male / Q000188:drug therapy / Q000378:metabolism; D007985:Leydig Cells / Q000378:metabolism / Q000502:physiology*; D007986:Luteinizing Hormone / Q000097:blood*; D008297:Male; D008596:Menotropins / Q000627:therapeutic use; D009845:Oligospermia / Q000378:metabolism / Q000503:physiopathology*; D010960:Plasminogen Activators / Q000096:biosynthesis; D011962:Receptors, FSH / Q000378:metabolism; D011974:Receptors, LH / Q000378:metabolism; D012708:Sertoli Cells / Q000378:metabolism / Q000502:physiology*; D013091:Spermatogenesis; D013739:Testosterone / Q000097:blood*; D013973:Thyrotropin-Releasing Hormone
chemical_list: D006063:Chorionic Gonadotropin; D011962:Receptors, FSH; D011974:Receptors, LH; D013739:Testosterone; D013973:Thyrotropin-Releasing Hormone; D008596:Menotropins; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D010960:Plasminogen Activators