Polycystic ovary syndrome (PCOS) is the most common endocrinopathies affecting the early reproductive age in women, whose pathophysiology perplexes many researchers till today. This syndrome is classically categorized by hyperandrogenism and/or hyperandrogenemia, menstrual and ovulatory dysfunction, bulky multi follicular ovaries on Ultrasonography (USG), and metabolic abnormalities such as hyperinsulinemia, dyslipidemia, obesity. The etiopathogenesis of PCOS is not fully elucidated, but it seems that the hypothalamus-pituitary-ovarian axis, ovarian, and/or adrenal androgen secretion may contribute to developing the syndrome. Infertility and poor reproductive health in women’s lives are highly associated with elevated levels of androgens. Studies with ovarian theca cells taken from PCOS women have demonstrated increased androgen production due to augmented ovarian steroidogenesis attributed to mainly altered expression of critical enzymes (Cytochrome P450 enzymes: CYP17, CYP21, CYP19, CYP11A) in the steroid hormone biosynthesis pathway. Despite the heterogeneity of PCOS, candidate gene studies are the widely used technique to delineate the genetic variants and analyze for the correlation of androgen biosynthesis pathway and those affecting the secretion or action of insulin with PCOS etiology. Linkage and association studies have predicted the relationship between genetic variants and PCOS risk among families or populations. Several genes have been proposed as playing a role in the etiopathogenesis of PCOS, and the presence of mutations and/or polymorphisms has been discovered, which suggests that PCOS has a vital heritable component. The following review summarizes the influence of polymorphisms in crucial genes of the steroidogenesis pathway leading to intraovarian hyperandrogenism which can result in PCOS.
PCOS is a prevalent endocrine disorder among women of reproductive age, characterized by hormonal imbalances and metabolic disturbances. This study explores the correlation between gut microbial β-glucuronidase and β-glucosidase and PCOS, focusing on their association with hormone levels and other clinical parameters. In this case-control study, fecal samples were collected from women of reproductive age, both with and without PCOS. The analysis of gut β-glucuronidase and β-glucosidase enzymes was conducted with the other clinical parameters, including body mass index, hormone levels, and hirsutism. These factors were then subjected to correlation analysis. PCOS women showed significantly higher levels of β-glucuronidase activity with a statistically significant P-value (0.05 ± 0.1 vs. 0.04 ± 0.1; P = 0.006) as well as β-glucosidase activity (0.13 ± 0.08 vs. 0.09 ± 0.05; P = 0.06) compared to the controls. This study also revealed intriguing connections between the selected enzymes and hormone levels, particularly testosterone and estradiol. Gut microbial enzymes β-glucuronidase and β-glucosidase may be used as biomarkers for early detection and monitoring of PCOS in women with metabolic challenges. It could lead to improved diagnostic tools and treatment options.
Objective: To identify Gut microbial β-Glucuronidase and β-Glucosidase activity in polycystic ovary syndrome (PCOS) and reveal a possible correlation between gut bacterial enzyme activities and estrogen. Design: Case-Control Study. Subjects: Reproductive-aged women with PCOS (n=23) and controls (n =25) from the Health Centre of Gujarat University. Interventions: Spectrophotometric analysis of β-Glucuronidase and β-Glucosidase activity of fecal samples from patients and clinical parameters (including body mass index, endocrine hormone levels, and hirsutism) collected for correlation analysis. Primary outcome: Identification of gut bacterial β-Glucuronidase and β-Glucosidase activity differences and clinical parameters. Results: Compared to the controls, PCOS women had considerably higher levels of β-glucuronidase activity, having statistically significant p-value (0.05 ± 0.1 vs. 0.04 ± 0.1; p= 0.006). We observed a higher trend of β-glucosidase activity in PCOS women compared to the control (0.13 ± 0.08 vs. 0.09 ± 0.05; p= 0.06). Conclusion: We observed a strong trend toward increased levels of β-glucuronidase and β-glucosidase activity in PCOS women compared to healthy control women. This inference requires further validation through studies with a larger sample size. However, if validated, we suggest that β-glucosidase levels can be considered a putative biomarker for PCOS women with metabolic disturbances and might help personalize the treatment.
Background: Polycystic ovary syndrome is a multifactorial endocrine disorder that affects reproductive-age women. Obesity and insulin resistance are well-known risk factors for PCOS. We investigated the frequency of rs9939609 in the FTO gene in women with PCOS and healthy controls and its relationship with metabolic traits and endocrine parameters in Gujarat province, India.Method We recruited 114 women (62 PCOS patients and 52 healthy controls). The genetic make-up of the rs9939609 polymorphisms in the FTO gene was conducted by tetra-primer amplification refractory mutation system-polymerase chain reaction.Results: The following genotype frequencies were found for rs9939609 in the FTO gene: Controls had 40.38% TT, 30.77% TA, and 28.85% AA, while cases had 43.55% TT, 19.35% TA, and 37.10% AA, with allele frequencies of 55.77% T allele and 44.23% A allele for controls and 53.23% T allele and 46.77% A allele for cases, respectively. The levels of total testosterone, DHEAS, and BMI were found to be statistically different between cases and controls. There were no differences in clinical variables between genotypes in the PCOS group.Conclusion There was no direct association between the rs9939609 FTO gene variant and PCOS in the study group, but it did have an impact on clinical features such as obesity and insulin resistance. According to our results, obese PCOS patients develop insulin resistance more often than nonobese PCOS patients.
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