Obesity and male fertility
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 througth different mechanisms, which alltogether could exert erectile dysfunction and/or sperm quality impa...
Guardado en:
Autores principales: | , , , |
---|---|
Formato: | Artículo revista |
Lenguaje: | Español |
Publicado: |
Universidad Nacional Cba. Facultad de Ciencias Médicas. Secretaria de Ciencia y Tecnología
2018
|
Materias: | |
Acceso en línea: | https://revistas.unc.edu.ar/index.php/med/article/view/21345 |
Aporte de: |
id |
I10-R10-article-21345 |
---|---|
record_format |
ojs |
institution |
Universidad Nacional de Córdoba |
institution_str |
I-10 |
repository_str |
R-10 |
container_title_str |
Revistas de la UNC |
language |
Español |
format |
Artículo revista |
topic |
obesidad sobrepeso fertilidad espermatozoide semen espermatogénesis eje hipotálamo-hipófiso-testicular leptina maduración epididimaria obesity overweight fertility spermatozoa semen spermatogenesis hypothalamic-pituitary-testicular axis leptin epididymal maturation |
spellingShingle |
obesidad sobrepeso fertilidad espermatozoide semen espermatogénesis eje hipotálamo-hipófiso-testicular leptina maduración epididimaria obesity overweight fertility spermatozoa semen spermatogenesis hypothalamic-pituitary-testicular axis leptin epididymal maturation Martini, Ana C. Molina, Rosa I. Ruiz, Rubén D. Fiol de Cuneo, Marta Obesity and male fertility |
topic_facet |
obesidad sobrepeso fertilidad espermatozoide semen espermatogénesis eje hipotálamo-hipófiso-testicular leptina maduración epididimaria obesity overweight fertility spermatozoa semen spermatogenesis hypothalamic-pituitary-testicular axis leptin epididymal maturation |
author |
Martini, Ana C. Molina, Rosa I. Ruiz, Rubén D. Fiol de Cuneo, Marta |
author_facet |
Martini, Ana C. Molina, Rosa I. Ruiz, Rubén D. Fiol de Cuneo, Marta |
author_sort |
Martini, Ana C. |
title |
Obesity and male fertility |
title_short |
Obesity and male fertility |
title_full |
Obesity and male fertility |
title_fullStr |
Obesity and male fertility |
title_full_unstemmed |
Obesity and male fertility |
title_sort |
obesity and male fertility |
description |
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 througth 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. |
publisher |
Universidad Nacional Cba. Facultad de Ciencias Médicas. Secretaria de Ciencia y Tecnología |
publishDate |
2018 |
url |
https://revistas.unc.edu.ar/index.php/med/article/view/21345 |
work_keys_str_mv |
AT martinianac obesityandmalefertility AT molinarosai obesityandmalefertility AT ruizrubend obesityandmalefertility AT fioldecuneomarta obesityandmalefertility AT martinianac impactodelaobesidadenlafuncionreproductivamasculina AT molinarosai impactodelaobesidadenlafuncionreproductivamasculina AT ruizrubend impactodelaobesidadenlafuncionreproductivamasculina AT fioldecuneomarta impactodelaobesidadenlafuncionreproductivamasculina |
first_indexed |
2022-08-20T01:25:49Z |
last_indexed |
2022-08-20T01:25:49Z |
_version_ |
1770718950386040832 |
spelling |
I10-R10-article-213452019-05-10T12:42:35Z Obesity and male fertility Impacto de la obesidad en la función reproductiva masculina Martini, Ana C. Molina, Rosa I. Ruiz, Rubén D. Fiol de Cuneo, Marta obesidad sobrepeso fertilidad espermatozoide semen espermatogénesis eje hipotálamo-hipófiso-testicular leptina maduración epididimaria obesity overweight fertility spermatozoa semen spermatogenesis hypothalamic-pituitary-testicular axis leptin epididymal maturation 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 througth 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. 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. Universidad Nacional Cba. Facultad de Ciencias Médicas. Secretaria de Ciencia y Tecnología 2018-09-17 info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion text/html https://revistas.unc.edu.ar/index.php/med/article/view/21345 Revista de la Facultad de Ciencias Médicas de Córdoba.; Vol. 69 No. 2 (2012); 102-110 Revista de la Facultad de Ciencias Médicas de Córdoba; Vol. 69 Núm. 2 (2012); 102-110 Revista da Faculdade de Ciências Médicas de Córdoba; v. 69 n. 2 (2012); 102-110 1853-0605 0014-6722 10.31053/1853.0605.v69.n2 spa https://revistas.unc.edu.ar/index.php/med/article/view/21345/20856 Derechos de autor 2018 Universidad Nacional de Córdoba |