Impacto de la obesidad en la función reproductiva masculina

Autores/as

  • Ana C. Martini Consejo Nacional de Investigaciones Científicas y Tecnológicas (CONICET). Cátedra de Fisiología Humana, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba. Santa Rosa 1085, X5000ESU, Córdoba.
  • Rosa I. Molina Laboratorio de Andrología y Reproducción (LAR). Chacabuco 1123 PB, 5000, Córdoba, Argentina.
  • Rubén D. Ruiz Consejo Nacional de Investigaciones Científicas y Tecnológicas (CONICET). Cátedra de Fisiología Humana, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba. Santa Rosa 1085, X5000ESU, Córdoba.
  • Marta Fiol de Cuneo Consejo Nacional de Investigaciones Científicas y Tecnológicas (CONICET). Cátedra de Fisiología Humana, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba. Santa Rosa 1085, X5000ESU, Córdoba.

DOI:

https://doi.org/10.31053/1853.0605.v69.n2.21345

Palabras clave:

obesidad, sobrepeso, fertilidad, espermatozoide, semen, espermatogénesis, eje hipotálamo-hipófiso-testicular, leptina, maduración epididimaria

Resumen

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.

Citas

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Publicado

2018-09-17

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1.
Martini AC, Molina RI, Ruiz RD, Fiol de Cuneo M. Impacto de la obesidad en la función reproductiva masculina. Rev Fac Cien Med Univ Nac Cordoba [Internet]. 17 de septiembre de 2018 [citado 18 de septiembre de 2021];69(2):102-10. Disponible en: https://revistas.unc.edu.ar/index.php/med/article/view/21345

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