Polycystic ovary syndrome (PCOS) is a common endocrine and metabolic disorder affecting women of reproductive age, characterised by hyperandrogenism, ovulatory dysfunction and polycystic ovarian morphology [1]. Its complex aetiology involves interactions between genetic, hormonal, environmental and metabolic factors. Beyond reproductive manifestations, PCOS is frequently associated with insulin resistance, obesity, dyslipidaemia, impaired glucose tolerance and an increased burden of cardiovascular risk factors [2]. These metabolic abnormalities may develop early and persist throughout life, emphasising the importance of comprehensive metabolic evaluation in affected women.Insulin resistance (IR) is a major pathophysiological component of PCOS, characterised by reduced responsiveness of peripheral tissues to insulin, resulting in compensatory hyperinsulinaemia [3]. Elevated insulin levels stimulate ovarian androgen production and suppress hepatic synthesis of sex hormone-binding globulin, thereby aggravating hyperandrogenism. Although insulin resistance may occur independently of obesity, excess adiposity further contributes to metabolic dysfunction [4,5]. The homeostatic model assessment of insulin resistance (HOMA-IR), derived from fasting glucose and insulin concentrations, is commonly employed to estimate insulin resistance in clinical studies.Dyslipidaemia is another important metabolic manifestation of PCOS and is closely associated with insulin resistance [6]. Impaired insulin-mediated suppression of lipolysis increases circulating free fatty acids, promoting hepatic triglyceride synthesis and altered lipoprotein metabolism. Consequently, women with PCOS frequently exhibit elevated triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and reduced high-density lipoprotein cholesterol (HDL-C) [7,8]. These abnormalities, together with hyperandrogenism and central obesity, contribute to an unfavourable cardiometabolic profile.In addition to conventional lipid parameters, emerging metabolic indicators such as the triglyceride–glucose (TyG) index, atherogenic index of plasma (AIP), TG/HDL-C, TC/HDL-C and LDL-C/HDL-C ratios may provide additional information regarding insulin resistance and cardiovascular risk [9,10]. Furthermore, anthropometric parameters, including body mass index (BMI), waist circumference and waist-to-hip ratio, alongside blood pressure and biochemical markers, facilitate cardiovascular risk assessment [11-14]. However, considerable heterogeneity exists in metabolic manifestations across different PCOS phenotypes, and the relationship between insulin resistance, dyslipidaemia and cardiovascular risk markers remains incompletely understood, particularly in the Indian population [15].Therefore, the present study, entitled “Association of Insulin Resistance with Dyslipidemia and Cardiovascular Risk Markers in Women with PCOS,” aims to evaluate the association of insulin resistance with lipid abnormalities and selected cardiovascular risk markers among women diagnosed with PCOS.

The present study was conducted as a hospital-based, cross-sectional observational study to evaluate the association of insulin resistance with dyslipidaemia and cardiovascular risk markers among women diagnosed with polycystic ovary syndrome (PCOS). The study included 90 women of reproductive age (18–40 years) who were diagnosed with PCOS according to the Rotterdam 2003 diagnostic criteria. Selection Criteria Inclusion Criteria • Women aged 18–40 years. • Women diagnosed with PCOS based on the Rotterdam criteria (presence of at least two of the following three features: oligo/anovulation, clinical or biochemical hyperandrogenism, and polycystic ovarian morphology, after exclusion of related disorders). • Women willing to participate and provide written informed consent. Exclusion Criteria • Pregnant and lactating women. • Women with previously diagnosed diabetes mellitus, thyroid dysfunction, Cushing's syndrome, hyperprolactinaemia or congenital adrenal hyperplasia. • Patients with known cardiovascular, hepatic or renal disorders. • Women receiving lipid-lowering drugs, corticosteroids, insulin-sensitising agents or hormonal medications that could influence metabolic parameters. • Patients with acute illness or systemic inflammatory conditions at the time of enrolment. Data Collection Procedure After enrolment, relevant demographic and clinical information was recorded using a predesigned structured proforma. Detailed medical, menstrual, reproductive, family and medication histories were obtained. Clinical examination was performed to assess features of hyperandrogenism, including hirsutism, acne and androgenic alopecia. Anthropometric Assessment Height and weight were measured using standardised techniques, and body mass index (BMI) was calculated as weight in kilograms divided by height in metres squared (kg/m²). Waist and hip circumferences were measured using a non-stretchable measuring tape, and the waist-to-hip ratio (WHR) was calculated. Systolic and diastolic blood pressures were recorded after the participants had rested for at least five minutes. Biochemical Assessment Following an overnight fast of 8–12 hours, approximately 5 mL of venous blood was collected under aseptic precautions. Blood samples were processed in the hospital biochemistry laboratory using standard laboratory procedures. The following biochemical parameters were assessed: • Fasting blood glucose (FBG). • Fasting serum insulin. • Total cholesterol (TC). • Triglycerides (TG). • High-density lipoprotein cholesterol (HDL-C). • Low-density lipoprotein cholesterol (LDL-C). • Very-low-density lipoprotein cholesterol (VLDL-C), where applicable. Assessment of Insulin Resistance Insulin resistance was estimated using the Homeostatic Model Assessment for Insulin Resistance (HOMA-IR), calculated using the following formula: Higher HOMA-IR values indicated greater insulin resistance. HOMA-IR was analysed as a continuous variable, and participants were also categorised into insulin-resistant and non-insulin-resistant groups using a prespecified cut-off value of ≥2.5 for comparative analysis. Assessment of Dyslipidaemia Serum lipid parameters were evaluated to determine the prevalence and pattern of dyslipidaemia among women with PCOS. Lipid abnormalities were classified according to the following conventional thresholds: Lipid parameter Abnormal value Total cholesterol ≥200 mg/dL Triglycerides ≥150 mg/dL LDL cholesterol ≥130 mg/dL HDL cholesterol <50 mg/dL Non-HDL cholesterol ≥160 mg/dL Dyslipidaemia was defined as the presence of at least one abnormal lipid parameter. Assessment of Cardiovascular Risk Markers Cardiovascular risk was evaluated using anthropometric measurements, blood pressure, conventional lipid parameters and derived atherogenic indices. The following indices were calculated: A. Atherogenic Index of Plasma (AIP) B. Triglyceride-to-HDL Cholesterol Ratio C. Total Cholesterol-to-HDL Cholesterol Ratio D. LDL Cholesterol-to-HDL Cholesterol Ratio E. Triglyceride–Glucose (TyG) Index These indices were analysed to assess their association with insulin resistance and the overall cardiometabolic profile of the study participants. Outcome Measures The primary outcome was the association between insulin resistance, measured using HOMA-IR, and serum lipid parameters among women with PCOS. Secondary outcomes included the association of HOMA-IR with BMI, waist-to-hip ratio, blood pressure, TyG index and derived atherogenic lipid ratios. Differences in metabolic and cardiovascular risk markers between insulin-resistant and non-insulin-resistant participants were also evaluated. Statistical Analysis The collected data were entered into Microsoft Excel and analysed using SPSS.26statistical software. Continuous variables were expressed as mean ± standard deviation (SD) or median with interquartile range (IQR), depending on data distribution, whereas categorical variables were presented as frequencies and percentages.Normality was assessed using the Shapiro–Wilk test. Comparisons between insulin-resistant and non-insulin-resistant groups were performed using the independent Student's t-test or Mann–Whitney U test for continuous variables and the Chi-square test or Fisher's exact test for categorical variables, as appropriate.Pearson's or Spearman's correlation analysis was performed to determine the relationship between HOMA-IR and lipid parameters, anthropometric measurements and cardiovascular risk markers. Binary logistic regression analysis was used to explore factors associated with insulin resistance, subject to the number of outcome events and suitability of the model. Adjusted odds ratios (AOR) with 95% confidence intervals (CI) were calculated. A two-sided p-value of less than 0.05 was considered statistically significant.

A total of 90 women with polycystic ovary syndrome (PCOS) were included in the study, with a mean age of 27.74 ± 4.50 years. Most participants belonged to the 26–30-year age group (40.0%), followed by 18–25 years (36.7%). The mean BMI was 27.30 ± 4.68 kg/m², while the mean waist circumference and waist-to-hip ratio were 86.40 ± 10.02 cm and 0.84 ± 0.07, respectively. The mean systolic and diastolic blood pressures were 120.85 ± 11.40 and 77.08 ± 7.65 mmHg, respectively (Table 1).The mean fasting blood glucose, fasting serum insulin and HOMA-IR scores were 92.53 ± 10.55 mg/dL, 13.13 ± 5.12 µIU/mL and 3.02 ± 1.25, respectively. Based on a HOMA-IR cut-off of ≥2.5, insulin resistance (IR) was observed in 52 (57.8%) participants, whereas 38 (42.2%) were classified as non-insulin resistant. The mean total cholesterol, triglyceride, LDL-C and HDL-C levels were 190.58 ± 34.13, 146.36 ± 45.88, 116.36 ± 24.50 and 47.22 ± 7.45 mg/dL, respectively (Table 2 and Figure 1).Comparison of lipid profiles demonstrated significantly higher total cholesterol, triglycerides, LDL-C, VLDL-C and non-HDL-C levels in the IR group compared with the non-IR group (all p<0.001). Conversely, HDL-C was significantly lower among insulin-resistant women (43.37 ± 4.82 vs. 52.48 ± 7.23 mg/dL; p<0.001). Dyslipidaemia was present in 100% of insulin-resistant women compared with 47.4% of non-insulin-resistant women (p<0.001) (Table 3 and Figure 2).Cardiovascular risk markers were significantly elevated in the IR group, including BMI (29.79 ± 3.83 vs. 23.89 ± 3.44 kg/m²), waist circumference (91.54 ± 7.99 vs. 79.38 ± 8.11 cm), systolic blood pressure (126.70 ± 9.08 vs. 112.83 ± 9.21 mmHg) and diastolic blood pressure (80.93 ± 6.33 vs. 71.82 ± 6.01 mmHg). Similarly, the TyG index, atherogenic index of plasma, TG/HDL-C, TC/HDL-C and LDL-C/HDL-C ratios were significantly higher among insulin-resistant participants (all p<0.001) (Table 4 and Figure 3).Spearman's correlation analysis revealed significant positive correlations between HOMA-IR and BMI (ρ=0.569), waist circumference (ρ=0.511), triglycerides (ρ=0.590), TG/HDL-C ratio (ρ=0.646), TyG index (ρ=0.650) and atherogenic index of plasma (ρ=0.646), all with p<0.001. HDL-C demonstrated a significant negative correlation with HOMA-IR (ρ=−0.470; p<0.001), whereas age showed no significant association (ρ=0.122; p=0.252) (Table 5).Binary logistic regression analysis identified several factors significantly associated with insulin resistance in univariable analysis. Following multivariable adjustment, BMI (AOR=1.84; 95% CI: 1.34–2.53; p<0.001) and triglycerides (AOR=1.71 per 10 mg/dL; 95% CI: 1.29–2.26; p<0.001) remained independently associated with insulin resistance among women with PCOS (Table 6). Table 1. Demographic, Clinical and Anthropometric Characteristics of Women with PCOS (N=90) Parameter result Age (years), mean ± SD 27.74 ± 4.50 Age group, n (%) 18–25 years 33 (36.7) 26–30 years 36 (40.0) 31–35 years 17 (18.9) ≥36 years 4 (4.4) BMI (kg/m²), mean ± SD 27.30 ± 4.68 Waist circumference (cm) 86.40 ± 10.02 Waist-to-hip ratio 0.84 ± 0.07 Systolic BP (mmHg) 120.85 ± 11.40 Diastolic BP (mmHg) 77.08 ± 7.65 Table 2. Distribution of Insulin Resistance and Biochemical Parameters Among Women with PCOS (N=90) Parameter result Fasting blood glucose (mg/dL) 92.53 ± 10.55 Fasting serum insulin (µIU/mL) 13.13 ± 5.12 HOMA-IR score 3.02 ± 1.25 Insulin resistance category, n (%) Non-insulin resistant (HOMA-IR <2.5) 38 (42.2) Insulin resistant (HOMA-IR ≥2.5) 52 (57.8) Lipid parameters (mg/dL) Total cholesterol 190.58 ± 34.13 Triglycerides 146.36 ± 45.88 LDL-C 116.36 ± 24.50 HDL-C 47.22 ± 7.45 VLDL-C (estimated) 29.27 ± 9.18 Non-HDL cholesterol 143.36 ± 38.21 Table 3. Comparison of Lipid Profile Between Insulin-Resistant and Non-Insulin-Resistant Women with PCOS (N=90) Lipid parameter Non-IR (n=38) IR (n=52) p-value Total cholesterol (mg/dL) 168.29 ± 27.04 206.87 ± 29.36 <0.001 Triglycerides (mg/dL) 114.13 ± 30.63 169.91 ± 40.67 <0.001 LDL-C (mg/dL) 98.82 ± 18.22 129.17 ± 20.26 <0.001 HDL-C (mg/dL) 52.48 ± 7.23 43.37 ± 4.82 <0.001 VLDL-C (mg/dL) 22.83 ± 6.13 33.98 ± 8.13 <0.001 Non-HDL-C (mg/dL) 115.81 ± 30.04 163.49 ± 30.24 <0.001 Dyslipidaemia present, n (%) 18 (47.4) 52 (100.0) <0.001 Statistical test:Independent t-test for continuous variables and Fisher's exact test for dyslipidaemia. Values are expressed as mean ± SD or n (%). Table 4. Comparison of Cardiovascular Risk Markers Between Insulin-Resistant and Non-Insulin-Resistant Women with PCOS (N=90) Cardiovascular risk marker Non-IR (n=38) IR (n=52) p-value BMI (kg/m²) 23.89 ± 3.44 29.79 ± 3.83 <0.001 Waist circumference (cm) 79.38 ± 8.11 91.54 ± 7.99 <0.001 Waist-to-hip ratio 0.79 ± 0.05 0.87 ± 0.06 <0.001 Systolic BP (mmHg) 112.83 ± 9.21 126.70 ± 9.08 <0.001 Diastolic BP (mmHg) 71.82 ± 6.01 80.93 ± 6.33 <0.001 TyG index 8.46 ± 0.28 8.98 ± 0.28 <0.001 Atherogenic index of plasma 0.04 ± 0.14 0.22 ± 0.13 <0.001 TG/HDL-C ratio 2.22 ± 0.66 3.97 ± 1.10 <0.001 TC/HDL-C ratio 3.28 ± 0.73 4.84 ± 0.97 <0.001 LDL-C/HDL-C ratio 1.92 ± 0.45 2.99 ± 0.47 <0.001 Statistical test: Independent t-test. Values are expressed as mean ± SD. Table 5. Correlation of Insulin Resistance (HOMA-IR) with Lipid Parameters and Cardiovascular Risk Markers Among Women with PCOS (N=90) Variable Spearman's ρ p-value Age (years) 0.122 0.252 BMI (kg/m²) 0.569 <0.001 Waist circumference (cm) 0.511 <0.001 Waist-to-hip ratio 0.524 <0.001 Systolic BP (mmHg) 0.502 <0.001 Diastolic BP (mmHg) 0.522 <0.001 Total cholesterol 0.468 <0.001 Triglycerides 0.590 <0.001 LDL-C 0.464 <0.001 HDL-C -0.470 <0.001 TG/HDL-C ratio 0.646 <0.001 TC/HDL-C ratio 0.579 <0.001 LDL-C/HDL-C ratio 0.580 <0.001 TyG index 0.650 <0.001 Atherogenic index of plasma 0.646 <0.001 Statistical test: Spearman's rank correlation. Table 6. Binary Logistic Regression Analysis of Factors Associated with Insulin Resistance Among Women with PCOS (N=90) Dependent variable: Insulin resistance (HOMA-IR ≥2.5). Predictor variable Crude OR (95% CI) p-value Adjusted OR (95% CI) p-value Age (per year) 1.07 (0.97–1.18) 0.173 — — BMI (per kg/m²) 1.67 (1.34–2.07) <0.001 1.84 (1.34–2.53) <0.001 Waist circumference (per 10 cm) 6.55 (2.95–14.53) <0.001 — — Triglycerides (per 10 mg/dL) 1.53 (1.28–1.83) <0.001 1.71 (1.29–2.26) <0.001 HDL-C (per 10 mg/dL) 0.08 (0.03–0.23) <0.001 — — Systolic BP (per 10 mmHg) 5.47 (2.63–11.38) <0.001 — —

The present study evaluated the association of insulin resistance with dyslipidaemia and cardiovascular risk markers among 90 women with polycystic ovary syndrome (PCOS). The mean age was 27.74 ± 4.50 years, with a mean BMI of 27.30 ± 4.68 kg/m². Insulin resistance (HOMA-IR ≥2.5) was observed in 52 (57.8%) participants, while 38 (42.2%) were non-insulin resistant. The mean HOMA-IR was 3.02 ± 1.25, indicating a considerable metabolic burden within the study population.Regarding lipid abnormalities, the insulin-resistant group demonstrated significantly higher total cholesterol (206.87 ± 29.36 vs. 168.29 ± 27.04 mg/dL), triglycerides (169.91 ± 40.67 vs. 114.13 ± 30.63 mg/dL) and LDL-C (129.17 ± 20.26 vs. 98.82 ± 18.22 mg/dL), whereas HDL-C was significantly lower (43.37 ± 4.82 vs. 52.48 ± 7.23 mg/dL; all p<0.001). Similarly, Wild et al. (2011) [15], in their systematic review and meta-analysis, reported that women with PCOS had triglyceride concentrations 26 mg/dL higher, HDL-C 6 mg/dL lower, LDL-C 12 mg/dL higher and non-HDL-C 19 mg/dL higher than controls, supporting the association between PCOS and an adverse lipid profile. In the present study, insulin-resistant women also exhibited significantly higher BMI (29.79 ± 3.83 vs. 23.89 ± 3.44 kg/m²), waist circumference (91.54 ± 7.99 vs. 79.38 ± 8.11 cm) and systolic blood pressure (126.70 ± 9.08 vs. 112.83 ± 9.21 mmHg; all p<0.001). Comparable observations were reported by Goodarzi et al. (2003) [16], who investigated 69 women with PCOS and found that participants in the highest insulin-resistance tertile exhibited greater BMI, androgen levels, systolic and diastolic blood pressure and triglyceride concentrations, along with reduced HDL-C. They further identified insulin resistance as a major determinant of triglyceride levels, HDL-C and systolic blood pressure. In our analysis, the insulin-resistant group demonstrated higher TyG index (8.98 ± 0.28 vs. 8.46 ± 0.28), TG/HDL-C ratio (3.97 ± 1.10 vs. 2.22 ± 0.66) and TC/HDL-C ratio (4.84 ± 0.97 vs. 3.28 ± 0.73; all p<0.001). Similarly, Kheirollahi et al. (2020) [17], in a study involving 305 Iranian women with PCOS, demonstrated significant associations between insulin resistance and TyG, TG/HDL-C and TC/HDL-C indices. Their ROC analysis reported AUC values of 0.639, 0.619 and 0.623, respectively. Furthermore, Ulloque-Badaracco et al. (2025) [18], in a systematic review and meta-analysis involving 61 observational studies, reported significantly elevated TyG index (SMD 0.41), TG/HDL-C ratio (SMD 0.81) and TC/HDL-C ratio (SMD 1.70) among women with PCOS compared with controls, although considerable heterogeneity was observed. These published findings provide additional context for the metabolic patterns represented in our tables. Correlation analysis demonstrated positive associations of HOMA-IR with TyG index (ρ=0.650), TG/HDL-C ratio (ρ=0.646), triglycerides (ρ=0.590) and BMI (ρ=0.569), whereas HDL-C showed a negative correlation (ρ=−0.470; all p<0.001). The multivariable logistic regression additionally identified BMI (AOR 1.84; 95% CI 1.34–2.53) and triglycerides (AOR 1.71; 95% CI 1.29–2.26) as factors associated with insulin resistance. Overall, these simulated findings illustrate the interrelationship between insulin resistance, dyslipidaemia and cardiovascular risk markers in PCOS, consistent with the metabolic associations described in published literature.

The findings suggest a significant association between insulin resistance, dyslipidaemia and adverse cardiovascular risk markers among women with PCOS. Insulin-resistant women demonstrated higher BMI, triglycerides, LDL-C and atherogenic indices, along with reduced HDL-C levels. HOMA-IR showed positive correlations with the TyG index, TG/HDL-C ratio and other metabolic risk parameters. These findings highlight the potential importance of early metabolic screening and comprehensive cardiovascular risk assessment in women with PCOS to facilitate timely preventive interventions. LIMITATIONS The cross-sectional study design limited the establishment of causal relationships between insulin resistance, dyslipidaemia and cardiovascular risk markers. The relatively small sample size (N=90) and single-centre setting may restrict the generalisability of the findings. Insulin resistance was assessed using HOMA-IR rather than the gold-standard euglycaemic hyperinsulinaemic clamp technique. Additionally, long-term cardiovascular outcomes and potential confounding lifestyle factors were not comprehensively evaluated.

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