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Glucocorticoids Stimulate the Accumulation of Lipids in the Rat Corpus Luteum¹

^a Departments of Internal Medicine, ^b Obstetrics and Gynecology, ^c Anatomy and Cell Biology, ^d Pharmacology, ^e Physiology, and ^f Reproductive Sciences Program, University of Michigan, Ann Arbor, Michigan 48109

We investigated the physiological basis for the trophic effect of glucocorticoids in rat corpora lutea in the absence of pituitary gonadotropins. Immature (Day 29) Sprague-Dawley rats were given eCG and hCG to induce the development 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 µg/rat/day) or vehicle (controls) and then were killed on Day 44. Plasma 20-dihydroprogesterone, a major steroid produced by the corpora lutea, was higher (p 0.01) in dex-treated than in control rats (44.5 ± 2.3 vs. 23.0 ± 5.6 ng/ml). Dexamethasone treatment increased lipid droplets and lipid in the corpora lutea as revealed by electron microscopy and oil red O staining. Cholesterol esters were higher in corpora lutea of dex-treated rats compared to controls (14.8 ± 1.1 vs. 2.2 ± 0.5 µg/mg corpora lutea wet tissue, respectively; p 0.05). Another group of hypophysectomized rats was treated with either a high or a lower dosage of corticosterone, both of which caused an elevation to > 2-fold of plasma 20-dihydroprogesterone concentration compared to controls. Glucocorticoid receptor protein (about 92 kDa) was detected in both luteal and nonluteal ovarian tissues in this animal model. These effects of glucocorticoids and the presence of the glucocorticoid receptor raise the possibility of a physiological role for glucocorticoids in the rat corpus luteum.

¹ Supported by NIH Grants HD33478 (P.L.K.) and P30 HD18258 Morphology Core and Assay and Reagents Core Facilities, by a Summer Biomedical Fellowship of the Undergraduate Research Opportunity Program of the University of Michigan (J.M.C.), and by a Rackham Predoctoral Fellowship of the University of Michigan (J.M.B.).

² Correspondence: R. Towns, Department of Internal Medicine, Division of Endocrinology and Metabolism, University of Michigan Medical School, 1331 E. Ann St., Room 5111, Ann Arbor, MI 48109-0580. FAX: 734 647 2307; rtowns{at}umich.edu

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