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Effects of Leydig cell-specific Esr1 deletion on male reproduction in mice
Estrogen plays an important role both in male and female reproduction. Two estrogen receptor isoforms, Esr1 and Esr2, are expressed in male gonad. In the mouse, Esr1 is expressed in Leydig cells of testis and pituitary. Esr1-/- male mice show enhanced androgen synthesis, spermatogenic defect, and infertility. To evaluate the specific function of Esr1 in Leydig cells, we examined spermatogenesis and steroidogenesis in Esr1f/fCyp17iCre male mice in which Esr1 is deleted specifically in Leydig cells. These mice showed normal spermatogenesis and fertility when compared to wild type from young adulthood to old age. Testosterone synthesis in Esr1f/fCyp17iCre mice at 3-12 months old of age was not different from age-matched wild type mice, while, at 18 months old of age, circulating testosterone concentrations were significantly higher than wild type together with increased levels of Star, Cyp17a1, and Hsd17b3 mRNA and with a hypertropy of Leydig cells. In Esr1f/fCyp17iCre mouse pituitaries, Fshb and Lhb mRNA levels were not different from wild type from young adulthood to old age. Taken together, Esr1 in Leydig cells may be not essential for spermatogenesis and fertility under control of endogenous estrogens and may have a role in aged Leydig cell function.
