Altered corticosterone status impairs steroidogenesis in the granulosa and thecal cells of Wistar rats.
Hypo- and hyper-corticosteronisms have adverse effects on ovarian endocrine and exocrine functions. In the present study, the mechanism by which corticosterone in excess or insufficiency impairs steroidogenesis in granulosa and thecal cells was investigated in adult albino Wistar rats. In this regard, rats were administered with corticosterone-21-acetate (2 mg/100 g b.wt., s.c., twice daily) or metyrapone (11beta-hydroxylase blocker) (10 mg/100 g b.wt., s.c., twice daily) for 15 days and a group of corticosterone/metyrapone treated rats was withdrawn of treatment and maintained for another 15 days and killed during their diestrus phase. Administration of corticosterone-21-acetate while elevated the serum corticosterone levels, metyrapone diminished the same. Administration of metyrapone reduced the serum levels of LH and estradiol; corticosterone reduced the levels of FSH in addition to LH and estradiol. In vitro production of progesterone and estradiol by the granulosa and thecal cells was decreased due to altered corticosterone status. Whereas administration of corticosterone significantly reduced the activity of 3beta-hydroxysteroid dehydrogenases (3beta-HSD) in granulosa and thecal cells, it reduced the activity of 17beta-HSD only in granulosa cells. While metyrapone treatment reduced the activity of 17beta-HSD in granulosa as well as thecal cells, it reduced the activity of 3beta-HSD only in thecal cells. The findings of the present investigation clearly demonstrate that excess or insufficiency in corticosterone affects steroidogenic process in the ovary. This is achieved by decreasing the levels of gonadotropins probably by their diminished synthesis and secretion and by interfering at the signal transduction process of these gonadotropins.
Department of Endocrinology, Dr. ALM PG Institute of Basic Medical Sciences, University of Madras, Taramani, Chennai, India.
G
G
Valli
S
S
Sudha
B
B
Ravi Sankar
P
P
Govindarajulu
N
N
Srinivasan
D015067:17-Hydroxysteroid Dehydrogenases / Q000378:metabolism; D000818:Animals; D001835:Body Weight; D003345:Corticosterone / Q000097:blood* / Q000494:pharmacology; D004958:Estradiol / Q000097:blood; D004971:Estrus; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood / Q000378:metabolism; D006107:Granulosa Cells / Q000201:enzymology / Q000378:metabolism*; D007986:Luteinizing Hormone / Q000097:blood / Q000378:metabolism; D008797:Metyrapone / Q000494:pharmacology; D009929:Organ Size; D011374:Progesterone / Q000097:blood; D011485:Protein Binding; D051381:Rats; D017208:Rats, Wistar; D013256:Steroids / Q000096:biosynthesis*; D013799:Theca Cells / Q000201:enzymology / Q000378:metabolism*
D013256:Steroids; D011374:Progesterone; D004958:Estradiol; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D015067:17-Hydroxysteroid Dehydrogenases; C044256:3 (or 17)-beta-hydroxysteroid dehydrogenase; D003345:Corticosterone; D008797:Metyrapone