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1.
Biol Reprod ; 50(6): 1394-402, 1994 Jun.
Article in English | MEDLINE | ID: mdl-8080927

ABSTRACT

There is an increase in plasma concentrations of immunoreactive (ir) inhibin unaccompanied by a rise in plasma progesterone during early pregnancy in the marmoset monkey. We investigated the potential involvement of hCG and prostaglandin E2 (PGE2) in stimulating a selective increase in inhibin concentrations by measuring the production of ir-alpha-inhibin and progesterone by dispersed luteal cells cultured under serum-free conditions. After one day, hCG had no effect on progesterone production by the cells but stimulated a significant increase (p < 0.05) in alpha-inhibin production. PGE2 significantly increased progesterone production (p < 0.001) but inhibited the production of alpha-inhibin (p < 0.001). After three days of culture, output of alpha-inhibin fell to low levels and no significant effect of hCG or PGE2 was detected. Progesterone also fell with time in culture, but hCG maintained production resulting in a significant increase above control levels (p < 0.001). The addition of low density lipoproteins (LDL) to the culture medium increased progesterone production (p < 0.001) while decreasing alpha-inhibin production (p < 0.01). Immunoneutralization of endogenous alpha-inhibin resulted in a significant decrease in both basal (p < 0.05) and gonadotropin-stimulated (p < 0.05) progesterone concentrations. These results provide further evidence for differential control of progesterone and alpha-inhibin production by marmoset luteal cells and show that hCG can selectively stimulate alpha-inhibin production. In addition, alpha-inhibin may have a local paracrine action in the marmoset CL, enhancing both basal and gonadotropin-stimulated progesterone secretion.


Subject(s)
Chorionic Gonadotropin/pharmacology , Inhibins/pharmacology , Luteal Cells/metabolism , Progesterone/biosynthesis , Animals , Callithrix , Cells, Cultured , Culture Media , Dinoprostone/pharmacology , Epidermal Growth Factor/pharmacology , Female , Follicle Stimulating Hormone/pharmacology , Lipoproteins, LDL/pharmacology , Luteal Cells/drug effects , Progesterone/blood , Time Factors
2.
Am J Primatol ; 32(3): 187-195, 1994.
Article in English | MEDLINE | ID: mdl-31936919

ABSTRACT

This study describes the peripheral concentrations of immunoreactive (ir) inhibin, progesterone, and bioactive gonadotrophin during pregnancy in the marmoset monkey, a New World primate. Blood samples were taken every two weeks from six animals from ovulation to parturition. Plasma ir-inhibin concentrations were measured by inhibin α-subunit-directed radioimmunoassay (RIA) and a recently developed two-site immunoradiometric assay (IRMA) which is specific for inhibin αß dimer. Concentrations of α-inhibin increased (P < 0.001) during early pregnancy to reach a peak on week 12 of pregnancy and showed a positive correlation with bioassayable gonadotrophin concentrations (r = 0.5, n = 64; P < 0.001). The concentrations of both α-inhibin and gonadotrophin showed no further peaks and declined (P < 0.001) to low levels prior to birth. Concentrations of dimeric inhibin were substantially lower than those measured by RIA and did not vary significantly during pregnancy. Progesterone concentrations remained at luteal-phase levels during the first half of pregnancy and increased (P < 0.05) during the second half to reach maximum concentrations just prior to birth. The relationship between α-inhibin, gonadotrophin, and progesterone suggests that the increase in α-inhibin may be luteal in source and under the control of gonadotrophin. The absence of a second increase in α-inhibin later in pregnancy and the finding that lategestation placenta contained very little α-inhibin differs from observations in Old World primates studied and suggests that the placenta may not be a source of inhibin during pregnancy in the marmoset. The finding of high levels of α-inhibin, but not dimeric inhibin, suggests that inhibin-related molecules may have a role other than suppression of pituitary folliclestimulating hormone. © 1994 Wiley-Liss, Inc.

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