Endocrine Abstracts

The incidence of obesity has dramatically increased, not only in industrialized societies but also in developing countries. Since male fertility shows a parallel decrease, obesity should be considered as possible etiology of male subfertility.

Studies exploring this possible association report that obesity may affect fertility by different mechanisms that include: abnormal reproductive hormonal milieu, increased release of adipokines and adipose-derived hormones (mainly leptin and resistin), in addition to other problems such as increased scrotal temperature, obstructive sleep apnea and accumulation of environmental toxins (endocrine disruptors) in adipose tissue. All these factors could provoke erectile dysfunction and/or decline in sperm quality.

Obese reproductive hormonal profile is characterized by reduced levels of total and free testosterone concentration, gonadotrophins, SHBG and/or inhibin B (marker of Sertoli cells function) and excess of estrogens (explained by the aromatase overactivity ascribed to adipose tissue increase).

The enhance in leptin levels could be responsible for at least some of the alterations on the hypothalamic-pituitary-testicular axis (reducing hypothalamic Kiss 1 expression) and could also exert direct deleterious effects on Leydig cells physiology, spermatogenesis and sperm function.

Adipokines (proinflammatory agents), higher scrotal temperature and toxins accumulation are responsible for the increase in testes oxidative stress, and sleep apnea suppresses the nocturnal testosterone rise necessary for normal spermatogenesis.

Finally, although controversial, hormonal misbalance and leptin increase might comprise gametes quality. Some reports indicate that obesity may decrease seminal sperm density/motility and increase sperm DNA fragmentation, probably disturbing spermatogenesis and/or epididymal function. Nonetheless, these alterations are mild.

In summary, although obesity may impair male fertility by some/all of the described mechanisms, the fact is that only a small proportion of obese men are infertile; probably those genetically predisposed or morbidly obese. Nevertheless, since the incidence of obesity is increasing, the number of men with reduced fertility will rise as well.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This work was supported, however funding details are unavailable.