Abstract
Previously, we reported that ESR1 overexpression resulting from neonatal exposure to estrogens in rats and wild-type mice was associated with infertility and mal-developed penis characterized by reduced length and weight and abnormal accumulation of fat cells. The objective of this study was to determine if mutant male mice overexpressing ESR1 are naturally infertile or have reduced fertility and/or develop abnormal penis. The fertility parameters, including fertility and fecundity indices, numbers of days from the day of cohabitation to the day of delivery, and numbers of pups per female, were not altered from controls, as a result of ESR1 overexpression. Likewise, penile morphology, including the length, weight, and diameter and os penis development, was not altered from controls. Conversely, weights of the seminal vesicles and bulbospongiosus and levator ani (BS/LA) muscles were significantly (P < 0.05) lower as compared to controls; however, the weight of the testis, the morphology of the testis and epididymis, and the plasma and testicular testosterone concentration were not different from controls. Hence, this study concludes that the genetically-induced ESR1 overexpression in male mice does not adversely affect fertility, penis, testis or epididymis, but significantly reduces weights of the seminal vesicles and BS/LA muscles. (poster)
Published Version
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