The Molecular Basis of Male Infertility in Obesity: A Literature Review
The rising incidence of obesity has coincided with rising levels of poor reproductive outcomes. The molecular basis for the association of infertility in obese males is now being explained through various mechanisms. Insulin resistance, hyperglycemia, and changes in serum and gonadal concentrations...
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| Format: | Article |
| Language: | English |
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MDPI AG
2023-12-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/25/1/179 |
| _version_ | 1797358705968152576 |
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| author | Biji Thomas George Malay Jhancy Rajani Dube Subhranshu Sekhar Kar Lovely Muthiah Annamma |
| author_facet | Biji Thomas George Malay Jhancy Rajani Dube Subhranshu Sekhar Kar Lovely Muthiah Annamma |
| author_sort | Biji Thomas George |
| collection | DOAJ |
| description | The rising incidence of obesity has coincided with rising levels of poor reproductive outcomes. The molecular basis for the association of infertility in obese males is now being explained through various mechanisms. Insulin resistance, hyperglycemia, and changes in serum and gonadal concentrations of adipokines, like leptin, adiponectin, resistin, and ghrelin have been implicated as causes of male infertility in obese males. The effects of obesity and hypogonadism form a vicious cycle whereby dysregulation of the hypothalamic–pituitary–testicular axis—due to the effect of the release of multiple mediators, thus decreasing GnRH release from the hypothalamus—causes decreases in LH and FSH levels. This leads to lower levels of testosterone, which further increases adiposity because of increased lipogenesis. Cytokines such as TNF-α and interleukins, sirtuins, and other inflammatory mediators like reactive oxygen species are known to affect fertility in obese male adults. There is evidence that parental obesity can be transferred through subsequent generations to offspring through epigenetic marks. Thus, negative expressions like obesity and infertility have been linked to epigenetic marks being altered in previous generations. The interesting aspect is that these epigenetic expressions can be reverted by removing the triggering factors. These positive modifications are also transmitted to subsequent generations. |
| first_indexed | 2024-03-08T15:05:56Z |
| format | Article |
| id | doaj.art-03400951e8a64d0299f426243a3c6f67 |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-08T15:05:56Z |
| publishDate | 2023-12-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | International Journal of Molecular Sciences |
| spelling | doaj.art-03400951e8a64d0299f426243a3c6f672024-01-10T14:58:27ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672023-12-0125117910.3390/ijms25010179The Molecular Basis of Male Infertility in Obesity: A Literature ReviewBiji Thomas George0Malay Jhancy1Rajani Dube2Subhranshu Sekhar Kar3Lovely Muthiah Annamma4Department of Surgery, RAK College of Medical Sciences, RAKMHSU, Ras al Khaimah P.O. Box 11172, United Arab EmiratesDepartment of Pediatrics, RAK College of Medical Sciences, RAKMHSU, Ras al Khaimah P.O. Box 11172, United Arab EmiratesDepartment of Obstetrics and Gynecology, RAK College of Medical Sciences, RAKMHSU, Ras al Khaimah P.O. Box 11172, United Arab EmiratesDepartment of Pediatrics, RAK College of Medical Sciences, RAKMHSU, Ras al Khaimah P.O. Box 11172, United Arab EmiratesDepartment of Clinical Sciences, Ajman University, Ajman P.O. Box 346, United Arab EmiratesThe rising incidence of obesity has coincided with rising levels of poor reproductive outcomes. The molecular basis for the association of infertility in obese males is now being explained through various mechanisms. Insulin resistance, hyperglycemia, and changes in serum and gonadal concentrations of adipokines, like leptin, adiponectin, resistin, and ghrelin have been implicated as causes of male infertility in obese males. The effects of obesity and hypogonadism form a vicious cycle whereby dysregulation of the hypothalamic–pituitary–testicular axis—due to the effect of the release of multiple mediators, thus decreasing GnRH release from the hypothalamus—causes decreases in LH and FSH levels. This leads to lower levels of testosterone, which further increases adiposity because of increased lipogenesis. Cytokines such as TNF-α and interleukins, sirtuins, and other inflammatory mediators like reactive oxygen species are known to affect fertility in obese male adults. There is evidence that parental obesity can be transferred through subsequent generations to offspring through epigenetic marks. Thus, negative expressions like obesity and infertility have been linked to epigenetic marks being altered in previous generations. The interesting aspect is that these epigenetic expressions can be reverted by removing the triggering factors. These positive modifications are also transmitted to subsequent generations.https://www.mdpi.com/1422-0067/25/1/179insulin resistancereproductive hormoneadipokineleptinadiponectinresistin |
| spellingShingle | Biji Thomas George Malay Jhancy Rajani Dube Subhranshu Sekhar Kar Lovely Muthiah Annamma The Molecular Basis of Male Infertility in Obesity: A Literature Review International Journal of Molecular Sciences insulin resistance reproductive hormone adipokine leptin adiponectin resistin |
| title | The Molecular Basis of Male Infertility in Obesity: A Literature Review |
| title_full | The Molecular Basis of Male Infertility in Obesity: A Literature Review |
| title_fullStr | The Molecular Basis of Male Infertility in Obesity: A Literature Review |
| title_full_unstemmed | The Molecular Basis of Male Infertility in Obesity: A Literature Review |
| title_short | The Molecular Basis of Male Infertility in Obesity: A Literature Review |
| title_sort | molecular basis of male infertility in obesity a literature review |
| topic | insulin resistance reproductive hormone adipokine leptin adiponectin resistin |
| url | https://www.mdpi.com/1422-0067/25/1/179 |
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