Analysis of the association between cytokine expression in the endometrial microenvironment and insulin resistance in polycystic ovary syndrome.

INTRODUCTION: Polycystic ovary syndrome (PCOS) is a common endocrine disorder in reproductive-aged women, often accompanied by insulin resistance (IR). The contribution of cytokines in the endometrial microenvironment to IR remains unclear. This study investigated their association in PCOS to identify potential clinical targets. METHODS: A case-control study involving 92 PCOS patients and 80 control subjects was conducted. Diagnosis followed the Rotterdam criteria. Insulin resistance was assessed by homeostasis model assessment of insulin resistance (HOMA-IR). Cytokines including TNF-α, IL-1β, IL-6, IL-8, IL-10, and MCP-1 in serum and uterine fluid samples were measured via enzyme-linked immunosorbent assay (ELISA). Logistic and linear regression models were utilized to evaluate associations between cytokine expression and insulin resistance. RESULTS: Compared with controls, PCOS patients showed higher FINS, TG, LDL, testosterone, AMH, HOMA-IR, LH, and BMI, and lower HDL (all P < 0.05). Serum and uterine fluid levels of IL-6, MCP-1, and TNF-α were significantly elevated in PCOS, while IL-8 showed no difference. Correlation analysis revealed that IL-6, MCP-1, and TNF-α were positively associated with HOMA-IR (all P < 0.05. Notably, logistic regression identified uterine fluid TNF-α as an independent predictor of insulin resistance (multivariate OR = 1.562, 95% CI: 1.151–2.122, P = 0.004). ROC analysis showed that uterine fluid TNF-α effectively predicted insulin resistance in PCOS (AUC = 0.81), outperforming IL-6 and MCP-1. CONCLUSIONS: Elevated uterine TNF-α in PCOS is closely linked to insulin resistance, highlighting the role of local inflammation in disease pathophysiology. Targeting TNF-α may offer a promising strategy to improve both metabolic and reproductive outcomes.