We investigated the physiological basis for the trophic effect of glucocort
icoids in rat corpora lutea in the absence of pituitary gonadotropins. Imma
ture (Day 29) Sprague-Dawley rats were given eCG and hCG to induce the deve
lopment of corpora lutea and were hypophysectomized on Day 32. Beginning on
Day 40, rats received twice-daily s.c. injections of either dexamethasone
(dex; 200 mu g/rat/day) or vehicle (controls) and then were kilted on Day 4
4. Plasma 20 alpha-dihydroprogesterone, a major steroid produced by the cor
pora lutea, was higher (p less than or equal to 0.01) in dex-treated than i
n control rats (44.5 +/- 2.3 vs. 23.0 +/- 5.6 ng/ml). Dexamethasone treatme
nt increased lipid droplets and lipid in the corpora lutea as revealed by e
lectron microscopy and oil red O staining. Cholesterol esters were higher i
n corpora lutea of dex-treated rats compared to controls (14.8 +/- 1.1 vs.
2.2 +/- 0.5 mu g/mg corpora lutea wet tissue, respectively; p less than or
equal to 0.05). Another group of hypophysectomized rats was treated with ei
ther a high or a lower dosage of corticosterone, both of which caused an el
evation to > 2-fold of plasma 20 alpha-dihydroprogesterone concentration co
mpared to controls. Glucocorticoid receptor protein (about 92 kDa) was dete
cted in both luteal and nonluteal ovarian tissues in this animal model. The
se effects of glucocorticoids and the presence of the glucocorticoid recept
or raise the possibility of a physiological role for glucocorticoids in the
rat corpus luteum.