Oestrogens in male reproduction

The role of oestrogens in male reproductive physiology is rapidly being redefined. While cases of oestrogen deficiency or insensitivity are rare among humans, insights are being gained from the development of mouse models in which oestrogen action has been abolished. Four knockout mouse models are currently available. The three oestrogen receptor knockout models—the oestrogen receptor-α (αERKO), -β (βERKO) and -αβ (αβERKO) double knockout mice—are providing valuable information on the loss of action of oestrogen receptors and the way in which either or both isoforms of the receptor are employed in any given action. On the other hand, the generation of the aromatase knockout (ArKO) mouse has produced animals unable to synthesize endogenous oestrogen. Fundamental perturbations that affect male fertility in these models include a disruption of testis morphology, an arrest of spermatogenesis at the stage of early spermiogenesis, a reduction in sperm concentration, motility and the ability to fertilize, severe dilatation of the efferent ductules and significant alterations to the normal hormone profile. The continuing accumulation of evidence from these animal models demonstrates that oestrogen plays an essential and direct role in the development and maintenance of male fertility.