Impact of obesity on male reproduction

MARTINI AC

Florencia

Congreso; 15th International and 14th European Congress of Endocrinology; 2012

The incidence of obesity has dramatically increased, not only in industrialized societies but also in developing countries. Since male fertility has parallely decreased, obesity should be considered as possible etiology of male subfertility. Studies exploring this possible association inform that obesity may affect fertility by different mechanisms that include: an abnormal reproductive hormonal milieu, increased release of adipokines and adipose derived hormones (mainly leptin and resistin) and other problems such as scrotal temperature increase, obstructive sleep apnea and environmental toxins (endocrine disruptors) accumulation 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 an 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 needed for normal spermatogenesis. Finally, although controversial, hormonal misbalance and leptin increase could comprise gametes quality. Some reports indicate that obesity may decrease seminal sperm density and motility and increase sperm DNA fragmentation, probably disturbing spermatogenesis and/or epididymal function. Nonetheless, these alterations are modest. 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 growing, the number of men with reduced fertility will increase as well.