Boars have high concentrations of plasma and testicular estrogens, but how this hormone is involved in feedback regulation of the gonadotropins and local regulation of testicular hormone production is unclear. The present study examined the effects of reducing endogenous estrogens by aromatase inhibition on concentrations of plasma LH and FSH and on testicular and plasma concentrations of testosterone (T) and immunoreactive inhibin (INH). Thirty-six littermate pairs of boars were used. One boar from each pair was assigned to the control group (vehicle); the other boar to the treatment group (aromatase enzyme inhibitor, Letrozole, 0.1 mg/kg body weight [BW]). Weekly oral treatment started at 1 wk of age and continued until castration at 2, 3, 4, 5, 6, 7, or 8 mo. Plasma concentrations of gonadotropins, INH, T, estradiol (E2), and estrogen conjugates (ECs) were determined. Testicular tissue was collected at castration for determination of INH and T and for confirmation of reduced aromatase activity. The acute effects of aromatase inhibition on gonadotropins were monitored in two adult boars treated once with Letrozole (0.1 mg/kg BW). Treatment with the aromatase inhibitor reduced testicular aromatase activity by 90% and decreased E2 and ECs without changing acute, long-term, or postcastration LH and FSH. Plasma T, testicular T, and circulating INH concentrations did not change. Testicular INH was elevated in treated boars compared with controls. In conclusion, estrogen does not appear to play a regulatory role on gonadotropin secretion in the developing boar. This is in direct contrast to findings in males of several other species.
The study presented herein was designed to test the hypothesis that reduced endogenous estrogen in the boar alters efferent duct morphology, epididymal morphology, and steroid receptor expression. Twenty-eight littermate pairs of boars were treated with Letrozole, an aromatase inhibitor, or with vehicle from 1 week of age until castration at 2 through 8 months. Efferent ducts and epididymides were examined for morphological development and steroid receptor expression. Efferent duct morphology was not different between control and Letrozole-treated animals at any examined age. Androgen receptor (AR), estrogen receptor a (ERa), and b (ERb) were expressed in the epithelial cells of the efferent ducts at all ages; expression was similar in control and treated animals. Morphological development of the caput and corpus was delayed in Letrozole-treated animals, but this delay was transient since morphology was similar between control and treated animals at 8 months. The cauda did not show a delay in development, but was more developed in treated animals at 2 months. AR, ERa, and ERb were expressed in all three epididymal regions; no difference was observed between control and treated animals. In summary, estrogen appears to be important for development of the epididymis; however, the cauda may be regulated differently than the caput and corpus. Results for the efferent ducts suggest that the normally high endogenous estrogens are not required for regulation of fluid reabsorption in the boar. It also suggests that any ER activation required for maintenance of efferent duct morphology and function is normal in Letrozole-treated boars.
The abundant production of testicular estrogens and the presence of both ESR1 and ESR2 within boar testes are consistent with a role for estrogen in testicular development and/or function in this species. This study was aimed at determining the role of endogenous estrogen in the regulation of testicular development and function, including the effects on testis weight, histology, sperm production (detergent-resistant spermatid numbers), Sertoli cell numbers, and Leydig cell volume in the boar. Twenty-eight littermate pairs of boars were assigned to groups as follows: 1 boar from each pair was assigned to the control group (vehicle) and the other was assigned to treatment and received 0.1 mg/kg body weight of an aromatase enzyme inhibitor (letrozole) orally each week beginning at 1 week of age until castration at 2, 3, 4, 5, 6, 7, or 8 months of age. Testes were weighed and testicular parenchyma was recovered for determination of histology and detergent-resistant spermatid numbers, and for determination of Sertoli cell number and Leydig cell volume by staining for GATA-4 and 17-a hydroxylase/17-20 lyase respectively. Testes of aromatase-inhibited boars initially exhibited delayed lumen formation, lower testicular weight, fewer detergentresistant spermatids, and fewer Sertoli cells, but by 7 to 8 months, these boars had recovered and had larger testes, more detergentresistant spermatids per testis, and more Sertoli cells. Total Leydig cell volume increased in proportion to testis size. Reducing endogenous estrogen is consistent with a delay in testicular maturation/puberty that allows for a longer window for the proliferation of Sertoli cells and maturation of Leydig cells, resulting in larger testes and higher spermatid production.
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