Exposure to estrogen mimicking the level of late pregnancy suppresses estrus subsequently induced by estrogen at the level of the follicular phase in ovariectomized shiba goats

Abstract

A high-estrogen environment during late pregnancy is suspected to cause postpartum silent ovulation, and progesterone (P4) is suggested to recover estrus. However, few attempts have been undertaken to elucidate the influence of these steroids on estrus by analyzing hormonal profiles. We investigated estrus and luteinizing hormone (LH) surges in ovariectomized goats (n=6) assigned to three treatments in a cross-over design. In groups 1 and 2, 200 μg/kg body weight/day estradiol benzoate (Dose-200 E2B) was administered for 14 days concurrent with P4 for 11 days, while in the control, saline solution and P4 were administered likewise. Ten days after the final administration of Dose-200 E2B, group 2 was treated with P4 for 8 days, and all groups were treated with 2 μg/kg body weight E2B (Dose-2 E2B) 20 days after the final administration of Dose-200 E2B (or saline solution). The proportion of cases expressing estrus after the administration of Dose-2 E2B was smaller (P<0.01) in group 1 than in the control (1/6, 3/6 and 6/6; groups 1 and 2 and the control, respectively). The proportions of cases generating LH surges did not differ (P>0.1) among the groups (5/6, 5/6 and 6/6; groups 1 and 2 and the control, respectively), but the peak concentrations in groups 1 and 2 (26.2 ± 14.7 and 11.3 ± 6.7 ng/ml) were lower (P<0.01) than those in the control (67.8 ± 19.4 ng/ml). These results demonstrated that elevation of plasma estrogen mimicking late pregnancy inhibits the subsequent estrus induced by estrogen simulating the follicular phase.

Fig. 1.

Summary of the experimental protocols showing a schematic representation of the treatments in the three groups (groups 1 and 2 and the control). The numbers under the lines indicate the days after the initiation of the treatments. The hatched bars represent the period of insertion of controlled internal drug-releasing devices containing 0.3 g progesterone. The single- and double-lined arrows represent administration of 200 µg/kg body weight and 2 µg/kg body weight estradiol benzoate (Dose-200 E₂B and Dose-2 E₂B). The solid dots designate administration of saline solution.

Fig. 2.

The peripheral concentrations of estradiol-17β (E₂-17β; top panel), progesterone (P₄; middle panel) and luteinizing hormone (LH; bottom panel) from the initiation of treatment with 200 µg/kg body weight estradiol benzoate (Dose-200 E₂B) or saline solution, and P₄ (day 0) to day 32, one day before treatment with 2 µg/kg body weight estradiol benzoate (Dose-2 E₂B) in group 1 (n=6), group 2 (n=6) and the control (n=6).

Fig. 3.

Profiles of estradiol-17β (E₂-17β; top panel), progesterone (P₄; middle panel) and luteinizing hormone (LH; bottom panel) for 48 h after administration of 2 µg/kg body weight estradiol benzoate (Dose-2 E₂B) on day 33 in group 1 (n=6), group 2 (n=6) and the control (n=6).