Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder connected with insulin resistance (IR), low-grade inflammation, dyslipidemia, and altered adipokine secretion. We evaluated serum levels of leptin, adiponectin, visfatin, resistin, IL-6, and TNF-α in 150 women with PCOS, stratified by IR status (IR, n = 76; non-IR, n = 74), and examined their associations with anthropometric, metabolic, hormonal, inflammatory, and atherogenic parameters. Anthropometric data included body weight, height, BMI, waist circumference, and waist-to-height ratio (WHtR), while IR was assessed using HOMA-IR and the Matsuda index. Serum adipokines were measured using ELISA, and lipid parameters and atherogenic indices—including non-HDL cholesterol, AIP, leptin/adiponectin, and adiponectin/resistin ratios—were calculated. Women with IR had higher levels of leptin, visfatin, resistin, and TNF-α, and lower levels of adiponectin. Leptin correlated positively with weight, WHtR, HOMA-IR, and atherogenic indices. Adiponectin showed the strongest and most consistent associations with anthropometric indices, HOMA-IR, and the Matsuda index. Resistin was linked to IR indices and IL-6, and visfatin correlated negatively with HDL-C and insulin sensitivity. In a multivariate general linear model, WHtR, but not HOMA-IR, remained independently associated with higher leptin levels and with atherogenic indices. These findings suggest that in PCOS, central adiposity rather than IR explains a substantial part of the adverse adipokine and inflammatory profile, thereby contributing to elevated cardiometabolic risk and highlighting the need for targeted treatment strategies.

Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder commonly linked to insulin resistance (IR), low-grade chronic inflammation, dyslipidemia, and altered adi-pokine secretion. This study aimed to assess serum concentrations of key adi-pokines—leptin, adiponectin, visfatin, and resistin—in women with PCOS, stratified by IR status, and to examine their relationship with anthropometric, metabolic, inflammatory, and atherogenic parameters. A total of 150 women diagnosed with PCOS were divided into two subgroups: with IR (n = 76) and without IR (n = 74). Serum adipokines were measured using ELISA, and atherogenic indices (TG/HDL-C, LDL-C/HDL-C, and AIP) were calculated from fasting lipid profiles. Anthropometric data included body weight, BMI, waist and hip circumferences, and waist-to-hip ratio. IR was evaluated using HOMA-IR, QUICKI, and the Matsuda index. Women with IR had significantly higher lep-tin, visfatin, and resistin levels, and lower adiponectin. Leptin correlated positively with HOMA-IR, body weight, and lipid ratios, while adiponectin showed inverse links to tri-glycerides, TG/HDL-C, and AIP. Resistin was positively related to IR indices, and visfatin showed a negative correlation with HDL-C and insulin sensitivity. These findings suggest that IR in PCOS is associated with a proinflammatory and atherogenic adipokine profile, potentially increasing cardiometabolic risk and guiding treatment approaches.

Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine–metabolic disorder associated with insulin resistance (IR), visceral adiposity, and increased cardiometabolic risk. The visceral adiposity index (VAI) is a validated surrogate marker of adipose tissue dysfunction, but its relationship with circulating neurotrophins and adipokine balance in PCOS remains incompletely understood. In this study, 100 women with PCOS were stratified into lower- (n = 50) and higher-risk (n = 50) groups according to VAI. Anthropometric measures, fasting glucose and insulin concentrations, lipid profile, and serum levels of brain-derived neurotrophic factor (BDNF), nerve growth factor-β (NGFβ), leptin, adiponectin, and resistin were assessed. HOMA-IR, adipokine ratios and atherogenic indices were calculated. Multivariate regression showed that BDNF was independently associated with VAI and non-HDL cholesterol, whereas NGFβ was independently linked to HDL cholesterol and estradiol, highlighting neurotrophin relationships with metabolic and endocrine parameters beyond general adiposity. Correlation heatmap and network analyses demonstrated interconnected clusters linking visceral adiposity, IR, dyslipidemia, adipokine imbalance, and neurotrophins, with the leptin/adiponectin ratio emerging as a central integrative marker. These findings suggest that within a PCOS population, VAI-defined cardiometabolic risk is associated with distinct neurotrophin–adipokine signatures, highlighting neurotrophin–adipokine networks underlying visceral adiposity-driven cardiometabolic and endocrine risk.

Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine–metabolic disorder as-sociated with insulin resistance (IR), visceral adiposity, and increased cardiometabolic risk. The visceral adiposity index (VAI) is a validated surrogate marker of adipose tissue dysfunction, but its relationship with circulating neurotrophins and adipokine balance in PCOS remains incompletely understood. In this study, 100 women with PCOS were strati-fied into lower- (n = 50) and higher-risk (n = 50) groups according to VAI. Anthropometric measures, fasting glucose and insulin concentrations, lipid profile, and serum levels of brain-derived neurotrophic factor (BDNF), nerve growth factor-β (NGFβ), leptin, adi-ponectin, and resistin were assessed. HOMA-IR, adipokine ratios and atherogenic indices were calculated. Multivariate regression revealed that BDNF was independently associ-ated with VAI and non-HDL-cholesterol, whereas NGFβ was independently associated with HDL-cholesterol and estradiol, indicating neurotrophin associations with metabolic and endocrine parameters independent of general adiposity. Correlation heatmap and network analyses demonstrated interconnected clusters linking visceral adiposity, IR, dyslipidemia, adipokine imbalance, and neurotrophins, with the leptin/adiponectin ratio emerging as a central integrative marker. These findings indicate that VAI-defined car-diometabolic risk in PCOS is accompanied by distinct and opposing neurotrophin–adipokine signatures, highlighting neurotrophin–adipokine networks underlying visceral adiposity-driven cardiometabolic and endocrine risk.

Development of polycystic ovary syndrome (PCOS) like phenotype in women with diabetes mellitus type 1 (DMt1) on intensified insulin treatment is related to the subcutaneous insulin administration and leads to clinical and biochemical hyperandrogenism. The aim of the study was to perform a comparative hormonal analysis of the hypothalamic-pituitary-gonadal (HPG) axis in women with DMt1 and PCOS and women with classic PCOS without diabetes. 83 women were included - 21 with DMt1 and PCOS and 62 with PCOS only. Basal levels of: luteinizing hormone (LH), follicle stimulating hormone (FSH), estradiol (E2), testosterone (Т), sex hormone biding globulin (SHBG), dehydroepiadrostenedion sulfate (DHEA-S), Androstendion (А4), Anti-Müllerian Hormone (AMH), Prolactin (Prl), Thyroid stimulating hormone (TSH), LH/FSH, free androgen index (FAI), calculated free testosterone (cFT) и bioavailable testosterone (BioT) were calculated. Women with DMt1 and PCOS demonstrated significantly higher E2 levels (p=0.039), but lower DHEA-S (p=0.024) and prolactin (p=0.019) concentrations. No statistically significant differences were observed regarding LH (p=0.950), FSH (p=0.084), LH/FSH (р=0.531), SHBG (p=0.170), AMH (0.633), as well as androgen levels: Т (р=0.995), FAI (р=0.0420), cFT (p=0.361), BioT (p=0.199) and А4 (р=0.254). Women with DMt1 and PCOS had hormonal profile similar to the classic PCOS in terms of gonadotropin levels, ovarian androgens and AMH.

Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine–metabolic disorder frequently associated with insulin resistance (IR) and increased cardiovascular risk. Soluble CD40 ligand (sCD40L) and soluble E-selectin (sE-selectin) are circulating biomarkers reflecting immune activation and endothelial dysfunction, respectively. However, their differential associations with IR in PCOS, particularly in the context of central obesity, remain incompletely understood. This cross-sectional study included 80 women with PCOS stratified according to waist-to-height ratio (WHtR > 0.50 vs. ≤0.50). Clinical, metabolic, hormonal, inflammatory, and endothelial parameters were evaluated. Correlation and multivariable regression analyses were performed to identify independent determinants of circulating sCD40L and sE-selectin. Women with central obesity exhibited significantly higher fasting insulin, homeostatic model assessment for insulin resistance (HOMA-IR), triglycerides, non-high-density lipoprotein (non-HDL) cholesterol, systolic blood pressure (SBP), and sE-selectin concentrations, together with lower HDL cholesterol. No significant differences were observed in tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), or sCD40L. In adjusted regression models, fasting glucose independently predicted sCD40L (β = −0.27, 95% confidence interval (CI): −0.50 to −0.04, p = 0.020), whereas fasting insulin emerged as the strongest determinant of sE-selectin (β = 0.41, 95% CI: 0.17 to 0.65, p < 0.001). These findings suggest distinct associations of immune and endothelial biomarkers with IR in PCOS. Assessment of sCD40L and sE-selectin may provide complementary information for early cardiometabolic risk stratification in affected women.