Impacto de la obesidad en la función reproductiva masculina
DOI:
https://doi.org/10.31053/1853.0605.v69.n2.21345Palabras clave:
obesidad, sobrepeso, fertilidad, espermatozoide, semen, espermatogénesis, eje hipotálamo-hipófiso-testicular, leptina, maduración epididimariaResumen
Tanto la obesidad como la infertilidad masculina han aumentado durante las últimas décadas por lo que se ha explorado una posible asociación entre estas patologías. Los estudios informan que la obesidad puede afectar la fertilidad del varón por diferentes mecanismos, los que en última instancia, pueden provocar disfunción eréctil y/o deteriorar la calidad espermática. Dichos mecanismos incluyen: 1) disrupción en la fisiología del eje hipotálamo-hipófiso-testicular (HHT): disminución en la concentración sérica de testosterona, gonadotrofinas, SHBG y/o inhibina B e hyperestrogenemia; 2) incremento en la liberación de hormonas derivadas del tejido adiposo, entre ellas leptina, que podrían alterar la fisiología del eje HHT y/o afectar directamente las células de Leydig y la espermatogénesis; 3) aumento de las adipoquinas (proinflamatorias), incremento de la temperatura escrotal y acumulación de disruptores endócrinos en los adipocitos; todos ellos responsables de un aumento en el estrés oxidativo testicular y 4) la apnea del sueño, frecuente en obesos, que suprime el pico nocturno de testosterona necesario para la espermatogénesis. Finalmente, si bien está discutido, estos mecanismos podrían alterar la espermatogénesis y/o la maduración epididimaria, disminuyendo así la concentración y la motilidad espermática y aumentando la fragmentación del ADN.En resumen, si bien la obesidad puede afectar la fertilidad masculina por algunos/todos los mecanismos mencionados, lo cierto es que sólo una pequeña proporción de obesos son infértiles; probablemente aquéllos con obesidad mórbida o genéticamente predispuestos. Sin embargo, ya que la incidencia de obesidad sigue aumentando, es de esperar que el número de hombres con sub/infertilidad también lo haga.
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