Silent information Regulators (SIRT1) gene stimulates antioxidants’ expression, repairs cells damaged by oxidative stress (OS), and prevents the cells’ dysfunction. In particular, the role of different Sirtuins, particularly SIRT1 in reproduction, has been widely studied over the past decade. Decreased SIRT 1 causes mitochondrial dysfunction by increasing Reactive Oxygen Species (ROS), lipid peroxidation, and DNA damage in both male and female gametes (Sperms and Oocytes), leading to infertility. In the female reproductive system, SIRT1 regulates proliferation and apoptosis in granulosa cells (GCs), and its down-regulation is associated with a reduced ovarian reserve. SIRT1 also modulates the stress response to OS in GCs by targeting a transcription factor vital for ovarian functions and maintenance. ROS-mediated damage to spermatozoa’s motility and morphology is responsible for 30–80% of men’s infertility cases. High levels of ROS can cause damage to deoxyribo nucleic acid (DNA) in the nucleus and mitochondria, lipid peroxidation, apoptosis, inactivation of enzymes, and oxidation of proteins in spermatozoa. SIRT 1 is a cardioprotective molecule that prevents atherosclerosis by modulating various mechanisms such as endothelial injury due to impaired nitric oxide (NO) production, inflammation, OS, and regulation of autophagy. SIRT 1 is abundantly expressed in tubular cells and podocytes. It is also found to be highly expressed in aquaporin 2 positive cells in the distal nephron suggesting its involvement in sodium and water handling. SIRT1 improves insulin resistance by reducing OS and regulating mitochondrial biogenesis and function. It also decreases adiposity and lipogenesis and increases fatty acid oxidation. So, its involvement in the multiple pathways ensures its unique role in reproductive and metabolic derangement mechanisms.

Male infertility is a major health problem worldwide. We investigated a possible association between leptin, obesity, hormonal interplay and male infertility. This cross‐sectional study of 313 males (178 infertile and 135 fertile) was carried out in 2017. The subjects were categorised by body mass index (BMI) and body fat percentage (BF%) into normal weight, overweight and obese. Significantly higher levels of BMI and BF% (p‐value < 0.001) and lower levels of FSH, LH, testosterone, and SHBG (p‐value < 0.001) were found in infertile males. However, no significant difference was observed in leptin levels (p‐value = 0.35). Leptin levels were significantly higher, and all the sex hormones were significantly lower (p‐value < 0.001) in obese subjects, whereas according to BF% only leptin, FSH and SHBG were significantly different. Leptin showed a significant positive correlation with BMI and BF% (p < 0.001). A strong positive link to serum testosterone was found with age, FSH, and LH (p < 0.001) and a negative one with BMI and BF% (p < 0.001). In mutivariable anlaysis, after adjusting for the other covariates, a significant association between FSH and testosterone (p‐value <0.001) was found. Serum leptin levels did not differ significantly in fertile and infertile groups, and no association was found with infertility. Furthermore, male obesity was found to be associated with infertility with the decrease in levels of sex hormones.

BackgroundThis study aimed to estimate stress markers, oxidative stress (OS), reproductive hormones and sperm parameters in male smokers and non-smokers and observe the impact of oxidative stress markers and smoking on sperm count, motility and morphology in a selected population of Karachi, Pakistan.MethodsThis cross-sectional study was conducted from July 2017 to July 2018 at Aga Khan University (AKU), in Karachi, Pakistan. The subjects were recruited from the Sindh Institute of Reproductive Medicine (SIRM), Karachi based on defined inclusion criteria. The subjects were categorized into fertile and infertile based on cut off values of sperm parameters as recommended by the WHO i.e., sperm count/ejaculate of 39 × 106/ml, sperm motility 40% and normal morphology 4%. Two hundred eleven fertile and 165 infertile male subjects were included in the study. Serum cortisol, adrenaline, superoxide dismutase (SOD), and glutathione peroxidase (GPX) were analyzed by ELISA kits. Data was analyzed on SPSS-22. A p-value of <0.05 was considered statistically significant.ResultsAge, Body Mass Index (BMI), and body fat were similar among smokers and non-smokers. Age was significantly lower, while mean BMI and body fat were significantly higher among infertile smokers vs. fertile smokers (p-value < 0.05). The testosterone levels were significantly reduced among smokers as compared to non- smokers (p-value < 0.05). The median cortisol levels were increased as well as GPX, and steroid hormone-binding globulin (SHBG) were significantly reduced among smokers as compared to non-smokers. Additionally, the same findings with a significant difference have also been observed among infertile smokers as compared to fertile smokers (p-value < 0.05). This study has shown that the semen parameters (total count, motility, and morphology) are decreased in infertile smokers as compared to infertile non-smokers. Furthermore, the multivariate analysis showed that smoking causes a significant decrease in sperm count and morphology but it did not have any significant effect on motility.ConclusionSmoking has a significant effect on fertility, specifically sperm count and normal morphology of sperm. This might be due to OS produced by smoking, which has devastating effects on semen parameters, thus reducing male fertility. Infertility specialist should counsel their patients about the ill effects of smoking on their fertility status and should advise maintaining a healthy lifestyle, including normal weight and avoiding smoking, to prevent future health problems. Hence smokers should quit smoking for their next generation.

Aim The correlation of subclinical hypothyroidism (SCH) and polycystic ovary syndrome (PCOS) is a still insufficiently explored entity. The aim of this study was to determine the correlation between SCH and PCOS along with the impact of SCH on metabolic and hormonal parameters in women with PCOS. Methodology This cross-sectional study was conducted at the Gynecology Outpatient Department of Ziauddin Hospital Kemari, Karachi, Pakistan, from June 2019 to December 2019. A total of 90 diagnosed cases of PCOS were enrolled in the study. A non-probability consecutive sampling technique was used. After taking informed consent, participants were evaluated through clinical interviews, a questionnaire, and anthropometric measurements. The participants underwent the following assessments, i.e., transabdominal ultrasonography, hormonal profile (free testosterone, follicle-stimulating hormone, luteinizing hormone), and fasting blood sugar. Participants were divided into two groups based on thyroid-stimulating hormone (TSH) into the euthyroid group and subclinical hypothyroid (SCH) group. The Mann-Whitney test was used for comparing the two groups. Results Our results showed a significant difference in weight, body mass index (BMI), insulin, homeostatic model assessment of insulin resistance (HOMA-IR), and TSH were found in the SCH group as compared to the euthyroid group. A significant correlation of TSH with waist-hip ratio (WHR), weight, body mass index (BMI), insulin, and the homeostatic model assessment of insulin resistance (HOMA-IR) in PCOS patients. Conclusion This study showed a significant correlation of subclinical hypothyroidism with polycystic ovary syndrome. We found subclinical hypothyroidism may aggravate the insulin resistance; therefore, PCOS patients must be screened with a thyroid profile.

Inam illahi et al. This is an open access article distributed under the terms of the Creative Commons Attribution License CC-BY 4.0., which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.