title: Oral progestin priming increases ovarian sensitivity to gonadotropin stimulation and improves luteal function in the cat.
abstract: As the only domesticated species known to exhibit both induced and spontaneous ovulation, the cat is a model for understanding the nuances of ovarian control. To explore ovarian sensitivity to exogenous gonadotropins and the influence of progestin priming, we conducted a study of queens that were down-regulated with oral progestin or allowed to cycle normally, followed by low or high doses of equine chorionic gonadotropin (eCG) and human chorionic gonadotropin (hCG). Our metrics included 1) fecal steroid metabolite profiles before and after ovulation induction, 2) laparoscopic examination of ovarian follicles and corpora lutea (CL) on Days 2 and 17 (Day 0 = hCG administration), and 3) ovariohysterectomy (Day 17) to assess CL progesterone concentrations, morphometrics, and histology. Reproductive tracts from time-matched, naturally mated queens (n = 6) served as controls. Every progestin-primed cat (n = 12) produced the desired response of morphologically similar, fresh CL (regardless of eCG/hCG dose) by Day 2, whereas 41.7% of unprimed counterparts (n = 12) failed to ovulate or had variable-aged CL suggestive of prior spontaneous ovulation (P < 0.05). The ovarian response to low, but not high, eCG/hCG was improved (P < 0.05) in primed compared to unprimed cats, indicating increased sensitivity to gonadotropin in the progestin-primed ovary. Progestin priming prevented hyperelevated fecal steroid metabolites and normalized CL progesterone capacity, but only when combined with low eCG/hCG. However, priming failed to prevent ancillary CL formation, smaller CL mass, or abnormal luteal cell density, which were common to all eCG/hCG-treated cats. Thus, the domestic cat exposed to eCG/hCG produces CL with structural and functional aberrations. These anomalies can be partially mitigated by progestin priming, possibly due to a protective effect of progestin associated with enhanced ovarian sensitivity to gonadotropins.
authors.affiliation: Center for Species Survival, Smithsonian Conservation Biology Institute, National Zoological Park, Front Royal, Virginia 22630, USA.
authors.forename: Rosemary A
authors.initials: RA
authors.lastname: Stewart
authors.forename: Katharine M
authors.initials: KM
authors.lastname: Pelican
authors.forename: Adrienne E
authors.initials: AE
authors.lastname: Crosier
authors.forename: Budhan S
authors.initials: BS
authors.lastname: Pukazhenthi
authors.forename: David E
authors.initials: DE
authors.lastname: Wildt
authors.forename: Mary Ann
authors.initials: MA
authors.lastname: Ottinger
authors.forename: JoGayle
authors.initials: J
authors.lastname: Howard
mesh_terms: D000284:Administration, Oral; D000818:Animals; D002415:Cats; D006063:Chorionic Gonadotropin / Q000008:administration & dosage / Q000009:adverse effects / Q000494:pharmacology*; D003338:Corpus Luteum / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004351:Drug Resistance / Q000187:drug effects*; D005243:Feces / Q000737:chemistry; D005260:Female; D005300:Fertility Agents, Female / Q000008:administration & dosage / Q000009:adverse effects / Q000494:pharmacology; D007044:Hysterectomy / Q000009:adverse effects / Q000662:veterinary; D008184:Luteal Cells / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D034461:Luteinization / Q000187:drug effects; D010052:Ovariectomy / Q000009:adverse effects / Q000662:veterinary; D010053:Ovary / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D010060:Ovulation / Q000187:drug effects* / Q000378:metabolism; D010062:Ovulation Induction / Q000009:adverse effects / Q000379:methods / Q000662:veterinary*; D011372:Progestins / Q000008:administration & dosage / Q000494:pharmacology*; D011897:Random Allocation; D013256:Steroids / Q000032:analysis
chemical_list: D006063:Chorionic Gonadotropin; D005300:Fertility Agents, Female; D011372:Progestins; D013256:Steroids