Year: 2001
Type: article
Abstract: We investigated ovarian steroidogenic enzyme gene expression in exogenous androgen induced polycystic ovaries (PCO) in rabbits.Twelve 3-month peripubertal, and seven 9-11 month reproductive aged New Zealand White female rabbits were divided into four treatment (Rx) groups: controls receiving saline only, testosterone (T) treated (6-10 mg/Rx), LHRH analog (L) treated (leuprolide depot 1.0-1.2mg/Rx), and T plus L treated (T+L).Animals in each group were administered the treatment IM every 2 to 3 weeks for 12-14 weeks.Serum T levels (every 1-3 wks) in T (127 ± 29 ng/dl) and T+L treated (144 ± 27 ng/dl) groups during the treatment period were unequivocally higher than the levels in controls (16 ± 6 ng/dl) and L treatment (22 ± 4 ng/dl) groups.Serum E 2 , LH and FSH levels (every 1-3 wks) showed no discernable differences between the groups.Microscopic examination of the L, T+L and T treated rabbit ovaries revealed a spectrum of PCO changes in comparison to the age-matched control ovaries, depicting marked interstitial hypercellularity and large cystic follicles in all except markedly decreased immature follicles and a few small cystic follicles in T treated peripubertal rabbits.Ovarian P450 cholesterol side-chain cleavage (P450scc) and 3β-hydroxysteroid dehydrogenase (3β-HSD) mRNA and protein levels in PCOs of T and T + L treated animals were similar to the age-matched control ovaries, while in L treated PCOs both P450scc and 3β-HSD mRNA and protein levels were increased.Thus excess T alone did not alter the ovarian steroidogenic enzyme gene expressions despite the morphology changes.The L treatment alone had a gonadotropin agonistic effect resulting in both PCO and increased ovarian steroidogenic enzyme gene expression.However, excess T abolished the L-mediated increased ovarian steroidogenic enzyme gene expression, indicating the presence of an inhibitory effect of T on L induced ovarian steroidogenic enzyme gene expression.These findings suggest that the pathogenic mechanism by which PCO is induced by extra-ovarian source of T differs from that induced by increased gonadotropic effect alone.
Source: Clinical Pediatric Endocrinology
DOI: 10.1297/cpe.10.17
Authors: Kotaro Iwamoto, J. Ian Mason, Jose Manaligod, K-Y Francis Pau, Harold G. Spies, Songya Pang
Language: English
Subfield: Reproductive Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
OpenAlex ID: W1963790061