Association of miR-21 Expression and hormonal disorder in woman with polycystic ovary syndrome

Inflammatory response and immunological alteration in polycystic ovary syndrome: An integrative case-control study

Association of ovarian inflammation and hormonal dysregulation: a candidate mechanism underlying polycystic ovary syndrome

Polycystic ovary syndrome (PCOS) is a common endocrine disorder characterized by female infertility, menstrual irregularities, and hormonal imbalance, leading to impaired reproductive health. Hyperandrogenemia is considered a central endocrine feature and a key contributor to PCOS pathophysiology. A dehydroepiandrosterone (DHEA)-induced mouse model was established to investigate transcriptomic alterations in granulosa cells (GCs) and their association with endocrine and inflammatory changes in PCOS. Model validation was performed using histological analysis (H&E staining), estrous cycle analysis, Western blotting of estrogen receptors (ERα and ERβ), and serum hormone profiling by ELISA. The PCOS model exhibited typical phenotypes, including polycystic ovarian morphology, estrous cycle arrest, and elevated testosterone (T), luteinizing hormone (LH), and LH/FSH ratios. Increased ERα expression was observed in ovarian GCs. RNA sequencing (RNA-seq) identified 161 differentially expressed genes, enriched in TNF signaling, NF-κB signaling, and steroid hormone biosynthesis pathways. In vitro, T-treated primary GCs showed increased ERα/ERβ ratio and enhanced pro-inflammatory signaling, with suppression of anti-inflammatory markers, consistent with in vivo findings. Overall, these findings support an association between endocrine alterations and inflammatory responses in ovarian GCs during PCOS. In conclusion, inflammatory factor expression in GCs was significantly associated with reproductive hormone dysregulation in PCOS, suggesting a potential hormone–inflammation interaction axis in the pathophysiology of PCOS.

An Exploratory Study on Transcriptomic Profiling of Circulating miRNA Associated with Hub Genes in the Development of Polycystic Ovary Syndrome

Pilot study results suggest potential miRNAs and their target pathway links with PCOS that need validation in larger cohorts for diagnostic or therapeutic applications need validation in larger cohorts for diagnostic or therapeutic applications.

Investigating the Roles of Follistatin and Sex Hormone- Binding Globulin in Polycystic Ovary Syndrome Pathogenesis: Implications for HOMA-IR and Hyperandrogenism

Introduction: Polycystic ovary syndrome (PCOS) is an endocrine disorder characterized by an imbalance of reproductive hormones that leads to anovulation and irregular menstruation. We aimed to evaluate serum levels of SHBG, follistatin and HSP-70, alongside HOMA-IR and hyperandrogenism markers, in PCOS vs. controls. Materials and Methods: Ninety women aged 15 to 45 years participated in this case-control study, with 45 diagnosed with polycystic ovary syndrome and 45 serving as controls. Blood samples were collected during the early follicular phase and analyzed using enzyme-linked immunosorbent assay (ELISA) to measure levels of SHBG, follistatin, HSP-70, anti-Müllerian hormone (AMH), luteinizing hormone (LH), follicle-stimulating hormone (FSH), insulin, prolactin, and testosterone. Results: Results showed that women with polycystic ovary syndrome had significantly higher levels of follistatin (5.37 ± 0.45 ng/ml), HSP-70 (16.49±2.79), AMH (2386.14 ± 530.09 pg/dL), LH (3.33 ± 0.75 ng/dL), testosterone (2.73 ± 0.51 ng/ml), prolactin (64.21 ± 11.66 ng/ml), and free androgen index (773.23 ± 152.41), fasting insulin (15.21 ± 5.41 μIU/ml), glycated hemoglobin (HbA1c) (6.01 ± 0.24%), and HOMA-IR (3.72 ± 1.44), with reduced SHBG (0.35 ± 0.03 ng/dL) and FSH (2.61 ± 0.61 ng/ml) (p≤0.01 for all). Conclusion: These findings suggest that decreased SHBG and increased follistatin and HSP-70 contribute to the hormonal and metabolic disturbances observed in polycystic ovary syndrome. Therefore, SHBG, follistatin and HSP-70 serve as useful biomarkers for the early diagnosis and prognosis of this condition.

Anti‐Müllerian Hormone and Metabolic–Hormonal Profiles in Women With and Without Polycystic Ovary Syndrome: A Population‐Based Study

ABSTRACT Introduction Evidence regarding age‐related variation in anti‐Müllerian hormone (AMH) and its associations with hormonal and metabolic parameters in women with polycystic ovary syndrome (PCOS), healthy women, and those with isolated PCOS features remains inconsistent. This study aimed to address these gaps using a cross‐sectional, population‐based approach. Methods A total of 883 women aged 18–45 years were categorized into three groups: PCOS (n = 124; Rotterdam criteria), suspicious (one PCOS criterion, n = 274), and healthy controls (n = 485). The coefficient of determination (R2) assessed age‐related AMH variation. Linear regression evaluated associations between AMH and hormonal and metabolic profiles. Age‐stratified multivariable logistic regression, adjusted for BMI, parity, and physical activity, examined associations between AMH and type 2 diabetes (T2DM), hypertension, metabolic syndrome (MetS), and dyslipidemia. Results Age explained nearly 40% of AMH variation in healthy women, but only 20% in those with PCOS. AMH was inversely correlated with BMI in healthy and suspicious groups, but not in PCOS. Among healthy women aged ≥ 35 years, higher AMH was associated with a 37% reduced likelihood of T2DM (OR: 0.63, 95% CI: 0.41–0.97). In contrast, among women with PCOS aged < 35 years, elevated AMH was associated with 2.6‐fold higher odds of MetS (OR: 2.6, 95% CI: 1.20–6.20). In the suspicious group, AMH correlated positively with free androgen index and prolactin. Conclusion AMH declines less with age in women with PCOS than in healthy women. Higher AMH may be protective against T2DM in older healthy women but indicates elevated metabolic risk in younger women with PCOS, suggesting that AMH may serve as a life‐course biomarker for metabolic risk stratification and personalized preventive strategies in women's healthcare.

ASSOCIATION OF FREE ANDROGEN INDEX WITH LOW-GRADE INFLAMMATION IN DIFFERENT PHENOTYPES OF POLYCYSTIC OVARY SYNDROME

Background: Polycystic ovary syndrome (PCOS) is a common endocrine disorder associated with hyperandrogenism, insulin resistance, and chronic low-grade inflammation. This study evaluated the relationship between free androgen index (FAI) and inflammation across different PCOS phenotypes. Methods: In this hospital-based cross-sectional study, 330 women with PCOS diagnosed according to the modified Rotterdam criteria were classified into four phenotypes (A–D). Serum C-reactive protein (CRP), FAI, and HOMA-IR were measured and compared among phenotypes using appropriate statistical analyses. Results: Phenotype A was the most common (51.2%) and showed the highest CRP, FAI, and HOMA-IR values. CRP levels differed significantly among phenotypes (P=0.014), with elevated CRP most frequently observed in phenotype A (50.3%). FAI was positively correlated with HOMA-IR (r=0.255, P<0.001), but neither FAI nor HOMA-IR showed a significant association with CRP. Multivariable analysis confirmed that FAI, HOMA-IR, BMI, and age were not independent predictors of CRP. Conclusion: Hyperandrogenic PCOS phenotypes exhibit greater inflammatory and metabolic disturbances; however, FAI is not independently associated with systemic inflammation. These findings suggest that inflammation in PCOS is multifactorial and varies across phenotypes.