Associations between asprosin, insulin resistance, and oxidative stress in adults with obesity

The global increase in obesity is strongly associated with insulin resistance (IR) and related metabolic impairments. Asprosin (ASP), a glucogenic adipokine induced by fasting, has recently emerged as a potential biomarker of IR and abnormal body composition. However, its physiological role in obesity remains incompletely understood. To evaluate the associations between serum ASP levels, IR indices, oxidative stress markers (OS), liver function and inflammation parameters, and body composition in overweight and obese adults during a standardized 4-hour oral glucose tolerance test (OGTT). This cross-sectional study included 150 adults categorized by BMI into three groups: control (CG; BMI < 25 kg/m²), overweight (O1; BMI > 25 kg/m²), and obese (O2; BMI > 30 kg/m²). Participants underwent dual-energy X-ray absorptiometry (DXA), including visceral adipose tissue quantification, bioelectrical impedance analysis (BIA), and biochemical assessment. Measurements included serum ASP, C-peptide, HbA1c, lipid profile, total oxidative capacity (TOC), total antioxidative capacity (TAC), liver transaminases (ALT, AST) and C-reactive protein (CRP). IR was assessed using HOMA-IR, QUICKI, Matsuda Index, TyG, and the composite TyG-WHR index as a proxy for hepatic IR. ASP levels were significantly higher in O1 and O2 compared with CG (p < 0.001), and in O2 compared with O1 (p < 0.01). ASP positively correlated with fat mass, TOC, HOMA-IR, TyG, TyG-WHR, ALT, and CRP, and negatively with muscle mass, total body water, resting metabolic rate, QUICKI, and Matsuda Index (p < 0.05). ASP is strongly associated with IR and adverse metabolic profiles in obesity. Its preferential correlation with hepatic IR markers (TyG-WHR, ALT, CRP) and fat mass suggests that ASP may primarily reflect liver-specific metabolic dysfunction rather than peripheral IR. These findings highlight ASP as a promising biomarker and potential therapeutic target in obesity-related metabolic disease.