title: Gonadotropin control of inhibin secretion and the relationship to follicle type and number in the hpg mouse.
abstract: Inhibin is secreted in two distinct heterodimeric forms, A and B, but the mechanism for the differential control of these two forms is unclear. To evaluate the relationship between secretion of inhibin forms and folliculogenesis, the effects of gonadotropins on inhibin concentrations were studied in parallel with stereological enumeration of ovarian follicle types in gonadotropin-deficient hypogonadal (hpg) female mice treated with recombinant human FSH (10 IU/day), hCG (1 IU/day), or both for 20 days. Treatment with FSH alone significantly increased blood concentrations of both inhibin A and inhibin B, whereas hCG alone had no effect on either inhibin. The combination of FSH and hCG further increased the concentration of inhibin A but had no effect on the concentration of inhibin B beyond that of FSH. The number of primordial follicles per ovary was significantly reduced in FSH-treated hpg mice, but was not affected by hCG treatment. Antral follicles were absent in the untreated hpg mice, present following treatment with FSH, and were present in only limited numbers following hCG treatment alone. Preovulatory follicles were observed only in the wild-type and combined FSH and hCG treatment groups. These results demonstrate that secretion of both inhibins is associated with the presence of antral follicles. Inhibin A secretion is increased by the presence of preovulatory follicles, whereas the concentration of inhibin B is not affected. The observed effects of gonadotropins on inhibin A and B secretion may be explained by corresponding gonadotropin effects on follicle development.
authors.affiliation: Department of Reproductive Medicine, Westmead Hospital, New South Wales, Australia. yuanw@westgate.wh.usyd.edu.au
authors.forename: Yuan
authors.initials: Y
authors.lastname: Wang
authors.forename: Helen
authors.initials: H
authors.lastname: Newton
authors.forename: Jenny A
authors.initials: JA
authors.lastname: Spaliviero
authors.forename: Charles M
authors.initials: CM
authors.lastname: Allan
authors.forename: Benjamin
authors.initials: B
authors.lastname: Marshan
authors.forename: David J
authors.initials: DJ
authors.lastname: Handelsman
authors.forename: Peter J
authors.initials: PJ
authors.lastname: Illingworth
mesh_terms: D000818:Animals; D002452:Cell Count; D006063:Chorionic Gonadotropin / Q000494:pharmacology; D004958:Estradiol / Q000378:metabolism; D005260:Female; D005640:Follicle Stimulating Hormone / Q000378:metabolism / Q000494:pharmacology; D006062:Gonadotropins / Q000172:deficiency / Q000378:metabolism* / Q000494:pharmacology; D007006:Hypogonadism / Q000378:metabolism / Q000473:pathology; D007265:Inhibins / Q000378:metabolism*; D007986:Luteinizing Hormone / Q000378:metabolism / Q000494:pharmacology; D051379:Mice; D008817:Mice, Mutant Strains; D009929:Organ Size; D006080:Ovarian Follicle / Q000166:cytology* / Q000502:physiology*; D010053:Ovary / Q000254:growth & development; D010060:Ovulation; D011374:Progesterone / Q000378:metabolism; D013997:Time Factors
chemical_list: D006063:Chorionic Gonadotropin; D006062:Gonadotropins; C422362:inhibin A; C422364:inhibin B; D011374:Progesterone; D004958:Estradiol; D007265:Inhibins; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone