Abstract / Summary
Background/Objectives: Low-grade chronic inflammation is recognized as part of the systemic profile of polyendocrine metabolic ovarian syndrome (PMOS, formerly polycystic ovary syndrome, PCOS), although whether this inflammatory signal tracks insulin resistance, adiposity, or both remains unclear. This study evaluated whether the triglyceride-glucose (TyG) index, a surrogate of insulin resistance, is associated with subclinical inflammation independently of body mass index (BMI) in women with PMOS. Methods: In this retrospective cross-sectional study of 150 women with PMOS, the TyG index was calculated from fasting triglycerides and glucose. C-reactive protein (CRP; standard assay) and the systemic immune–inflammation index (SII) were pre-specified primary markers; the neutrophil-, platelet-, and monocyte-to-lymphocyte ratios (NLR, PLR, and MLR) and the systemic inflammation response index (SIRI) were secondary. Associations were assessed using Spearman correlation and multivariable linear regression adjusted for age and BMI, with component, extended-adjustment, tertile, and BMI-interaction analyses. Results: The TyG index correlated with the homeostatic model assessment of insulin resistance (HOMA-IR) (rho = 0.45, p < 0.001) but not with BMI (rho = 0.03, 95% confidence interval [CI] −0.13 to 0.19, p = 0.71). After adjustment, each standard deviation (SD) increment in TyG was associated with a 21.7% higher SII (95% CI 17.0 to 26.6%; p < 0.001) and with a higher NLR, PLR, MLR, and SIRI (all corrected p ≤ 0.023), with no TyG × BMI interaction. Both triglyceride and glucose components contributed, fasting insulin was only weakly associated, and results were unchanged after further adjustment for hormonal and glycemic covariates. TyG was not associated with CRP (p = 0.53), which was associated only with BMI. Conclusions: In PMOS, the TyG index was associated with hemogram-derived inflammatory indices independently of BMI, a signal attributable to its triglyceride and glucose components rather than to fasting insulin, whereas standard-assay CRP tracked adiposity. These cross-sectional findings are hypothesis-generating.