Martini Ana C, Molina Rosa I, Ruiz Rubén D, Fiol de Cuneo Marta
Investigadores del Consejo Nacional de Investigaciones Científicas y Tecnológicas, Cátedra de Fisiología Humana, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Santa Rosa 1085, X5000ESU, Córdoba, Argentina.
Rev Fac Cien Med Univ Nac Cordoba. 2012;69(2):102-10.
Obesity and male infertility have increased in the last decades; therefore, a possible association between these pathologies has been explored. Studies inform that obesity may affect fertility through different mechanisms, which alltogether could exert erectile dysfunction and/or sperm quality impairment. These include: 1) hypothalamic-pituitary-testicular (HPG) axis malfunction: obese hormonal profile is characterized by reduction of testosterone, gonadotrophins, SHBG and/or inhibin B concentrations (marker of Sertoli cells function) and hyperestrogenemy (consequence of aromatase overactivity ascribed to adipose tissue increase); 2) increased release of adipose-derived hormones: leptin increase could be responsible for some of the alterations on the HPG axis and could also exert direct deleterious effects on Leydig cells physiology, spermatogenesis and sperm function; 3) proinflammatory adipokines augmentation, higher scrotal temperature (due to fat accumulation in areas surrounding testes) and endocrine disruptors accumulation in adiposites, all of these responsible for the increase in testes oxidative stress and 4) sleep apnea, frequent in obese patients, suppresses the nocturnal testosterone rise needed for normal spermatogenesis. Finally, although controversial, all the above mentioned factors could comprise gametes quality; i.e. decrease sperm density and motility and increase DNA fragmentation, probably disturbing spermatogenesis and/or epididymal function. 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, it is likely that because the incidence of obesity is growing, the number of men with reduced fertility will increase as well.
在过去几十年中，肥胖症和男性不育症的发病率均有所上升；因此，人们对这两种病症之间可能存在的关联进行了探索。研究表明，肥胖可能通过不同机制影响生育能力，这些机制共同作用可能导致勃起功能障碍和/或精子质量受损。这些机制包括：1）下丘脑-垂体-睾丸（HPG）轴功能紊乱：肥胖者的激素水平特征为睾酮、促性腺激素、性激素结合球蛋白（SHBG）和/或抑制素B浓度降低（支持细胞功能的标志物）以及雌激素过多（归因于脂肪组织增加导致的芳香化酶活性过高）；2）脂肪衍生激素释放增加：瘦素增加可能是HPG轴某些改变的原因，也可能对睾丸间质细胞生理、精子发生和精子功能产生直接有害影响；3）促炎脂肪因子增加、阴囊温度升高（由于睾丸周围区域脂肪堆积）以及内分泌干扰物在脂肪组织中的蓄积，所有这些都会导致睾丸氧化应激增加；4）肥胖患者中常见的睡眠呼吸暂停会抑制正常精子发生所需的夜间睾酮升高。最后，尽管存在争议，但上述所有因素都可能影响配子质量；即降低精子密度和活力，增加DNA碎片化，可能干扰精子发生和/或附睾功能。总之，尽管肥胖可能通过部分/所有上述机制损害男性生育能力，但事实上只有一小部分肥胖男性不育，可能是那些有遗传易感性或病态肥胖的人。然而，由于肥胖症的发病率在上升，生育能力下降的男性数量可能也会增加。
