Association of Serum Asprosin, Chemerin, and Omentin-1 Levels with Insulin Resistance and Oxidative Stress in Adults with Obesity: A Comparative Cross-Sectional Study

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Obesity disrupts adipokine secretion, insulin sensitivity, and redox homeostasis, yet the integrated relationships among asprosin, chemerin, omentin-1, and oxidative-stress markers have not been comprehensively evaluated in Iraqi adults. This comparative cross-sectional study therefore assessed serum asprosin, chemerin, and omentin-1 in relation to insulin resistance and oxidative stress in 100 adults recruited in Baghdad -- 50 with BMI-defined obesity and 50 normal-weight controls. Anthropometric indices, fasting glucose, insulin, lipid profile, thiobarbituric acid-reactive substances (TBARS) expressed as malondialdehyde (MDA) equivalents, total antioxidant capacity (TAC), total glutathione, and the three adipokines were measured; HOMA-IR was calculated. Primary group comparisons with effect sizes and 95\% confidence intervals were supplemented by exploratory subgroup, pooled-correlation, regression, and receiver operating characteristic analyses. Adults with obesity exhibited significantly higher BMI, waist circumference, fasting insulin, HOMA-IR, triglycerides, MDA-equivalents, asprosin, and chemerin, alongside lower HDL-cholesterol, TAC, total glutathione, and omentin-1 (all \(p < 0.001\)), with large effect sizes for HOMA-IR and all six adipokine-redox biomarkers. In exploratory subgroup analyses within the obesity group, fasting insulin, HOMA-IR, and MDA-equivalents remained significant after Bonferroni correction, whereas the asprosin difference was nominal. MDA-equivalents and asprosin retained positive coefficients in the age- and sex-adjusted biochemical covariation model. Overall, obesity was characterized by a coordinated pattern of elevated asprosin and chemerin, reduced omentin-1, heightened insulin resistance and TBARS-reactive lipid peroxidation, and diminished antioxidant defence. These cross-sectional, single-center associations are hypothesis-generating rather than diagnostic; they demonstrate internal coherence but do not establish causality, independent adiposity-related effects, or clinical utility. Prospective multicenter studies with balanced obesity subgroups, direct adiposity assessment, within-group and adiposity-adjusted models, and external validation are required before these biomarkers can be considered for clinical risk assessment or screening.