Reduced fetal androgen exposure compromises Leydig cell function in adulthood.

Abstract

Disruption of normal fetal development can influence functioning of organs and cells in adulthood. Circumstantial evidence suggests that subtle reductions in fetal androgen production may be the cause of adult male reproductive disorders due to reduced testosterone production. The mechanisms through which these fetal events affect adult testosterone levels are largely unknown. A recent paper of Kilcoyne et al. provides evidence that fetal reduction in androgen production or signaling results in a reduced Leydig stems cell number after birth and concomitant Leydig cell failure in adulthood. This implies that fetal androgen deficiency can lead to negative programming of adult Leydig cell (ALC) function, which may have implications for general health, aging, and longevity.