title: A selective monotropic elevation of FSH, but not that of LH, amplifies the proliferation and differentiation of spermatogonia in the adult rhesus monkey (Macaca mulatta).
abstract: BACKGROUND
  Unilateral orchidectomy in monkeys increases spermatogenesis in the remaining testis in association with elevated follicle-stimulating hormone (FSH) secretion and testicular testosterone. The present study examined the relative importance of FSH and testosterone in driving the primate testis toward its spermatogenic ceiling.
  
  
  METHODS
  Adult male rhesus monkeys were treated with a gonadotropin-releasing hormone receptor antagonist to inhibit endogenous FSH and luteinizing hormone (LH) secretion. The gonadotrophin drive to the testis was replaced with a pulsatile recombinant human FSH and LH infusion to maintain testicular volume and circulating testosterone and inhibin B at physiological levels. A selective monotropic elevation of FSH or LH that doubled the concentrations of inhibin B or testosterone, respectively, was then imposed for 4 weeks, each in a group of four monkeys. In a third group (n = 4), the gonadotrophin drive remained clamped at physiological levels. Bromo-deoxyuridine was administered 3 h prior to castration, and the effects of the monotropic hormone increments on germ cell number, S-phase labeling and degeneration were determined.
  
  
  RESULTS
  Increased FSH, but not LH, produced increases in testicular volume (P < 0.05), the proportion of A pale spermatogonia entering the cell cycle and the numbers of differentiated spermatogonia and more advanced germ cells (P < 0.05). Indexes for spermatogonia labeling and germ cell degeneration were not affected.
  
  
  CONCLUSIONS
  Under physiological conditions, circulating concentrations of FSH directly dictate sperm output of the primate testis by regulating the proportion of Ap spermatogonia in the growth fraction. An effect of FSH on survival of the first generation of differentiated B spermatogonia is not excluded.
authors.affiliation: Department of Cell Biology and Physiology, Center for Research in Reproductive Physiology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.
authors.forename: D R
authors.initials: DR
authors.lastname: Simorangkir
authors.forename: S
authors.initials: S
authors.lastname: Ramaswamy
authors.forename: G R
authors.initials: GR
authors.lastname: Marshall
authors.forename: C R
authors.initials: CR
authors.lastname: Pohl
authors.forename: T M
authors.initials: TM
authors.lastname: Plant
mesh_terms: D000818:Animals; D002454:Cell Differentiation; D049109:Cell Proliferation; D005640:Follicle Stimulating Hormone / Q000096:biosynthesis*; D006062:Gonadotropins / Q000378:metabolism; D007986:Luteinizing Hormone / Q000096:biosynthesis*; D008253:Macaca mulatta; D008297:Male; D011994:Recombinant Proteins / Q000378:metabolism; D013091:Spermatogenesis; D013093:Spermatogonia / Q000378:metabolism*; D013737:Testis / Q000378:metabolism; D013739:Testosterone; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D006062:Gonadotropins; D011994:Recombinant Proteins; D013739:Testosterone; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone