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F. C. HAGEMENAS, W. L. BAUGHMAN, G. W. KITTINGER, The Effect of Fetal Hypophysectomy on Placental Biosynthesis of Progesterone in Rhesus, Endocrinology, Volume 96, Issue 4, 1 April 1975, Pages 1059–1062, https://doi.org/10.1210/endo-96-4-1059
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Placental slices from intact rhesus fetuses were incubated without added substrate. The incubated tissue levels of progesterone (P4) differed according to the sex of the fetus. Slices from female placentas contained significantly more P4 than did those of males. The addition of pregnenolone (P5) to the incubation media caused tissue levels of P4 to increase 1.5 to 3 times control tissue levels for both female and male placentas. Moreover, the sex difference in P4 biosynthesis was eliminated by adding P5 to the incubations. Since control incubations of male placental tissue produced less P4 than those of females, the net increase in P4 synthesis with added P5 was greater for male than female placental tissue. These observations indicated that the step(s) in P4 biosynthesis which were affected by the fetal genotype lay between cholestrol and P5.
Incubation of placental slices derived from decapitated fetuses secreted significantly less P4 into the incubation medium than those of intact fetuses. Moreover, the sex difference in the media content of P4 was eliminated. However, decapitation did not eliminate the sex difference in the tissue content of P4 during control incubations. When P5 was added to the incubations, media and tissue levels of P4 increased significantly over control levels for placentas from both sexes. However, the addition of P5 to the incubations from decapitated males did not restore P4 production in the tissue or the medium to levels observed for intact males. However, this did occur when P5 was added to incubations from decapitated females. It appears that fetal decapitation decreased cholesterol side chain cleaving activity and Γ5-βhydroxy-steroid dehydrogenase content of the placenta. These data indicate that hormones of fetal origin may control P4 production by the placenta. (Endocrinology96: 1059, 1975
