Answers are grounded in this paper and cite their sources.
Corpora lutea of gestation were isolated as autografts under the renal capsule after ovariectomy on Days 2 or 4 of gestation. Exogenous progesterone was provided by a subcutaneous implant of solid steroid in a Silastic elastomer matrix. The CL grafts did not secrete enough estrogen to induce nidation, to prevent loss of uterine weight after ovariectomy, or to prevent placental hypertrophy. When testosterone was supplied directly to the grafts as an implant in Silastic, the grafted corpora lutea were able to form sufficient estrogen to induce nidation in 11/21 rats, and to prevent loss of uterine weight after ovariectomy; placental hypertrophy, a symptom of estrogen deficiency, was not prevented. Vaginal mucification could not be used as a test for estrogen since testosterone alone (without grafts) also caused it. It was concluded that the grafted tissue did not secrete estrogen, but could convert exogenous testosterone to estrogen. When the grafts were maintained in the presence of testosterone until the end of gestation, by exogenous progesterone, the luteal cells underwent a transformation to large pale cells and smaller dark cells. These transformed cells had no demonstrable 20α-hydroxysteroid dehydrogenase activity or cholesterol deposition. There was no evidence that testosterone or estrogen had a direct luteotrophic action in enhancing progesterone secretion.
No takes yet. Share an insight, caveat, or question.
Gibori et al. (1973) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: