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Life sciences · Journal article
Hormone Molecular Biology and Clinical Investigation · November 1, 2026
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Abstract Objectives Visceral obesity is closely linked to insulin resistance and cardiometabolic risk. Epicardial adipose tissue, commonly assessed by epicardial fat thickness (EFT), is a clinically relevant fat depot associated with early cardiac remodelling. Sclerostin, a bone-derived protein, may play a role in crosstalk between the skeleton and adipose tissue. However, its relationship with insulin resistance and cardiac visceral fat remains unclear. This study aimed to evaluate serum sclerostin levels and their association with insulin resistance and EFT in obese women. Methods This case-control study included 90 women (55 obese and 35 age-matched controls). Participants underwent anthropometric and metabolic assessment, including serum sclerostin measurement. Insulin resistance was evaluated using HOMA-IR, and EFT was assessed by echocardiography. Correlation, ROC, and regression analyses were performed. Results Serum sclerostin levels were significantly higher in obese women than in controls (p<0.001). Sclerostin was positively correlated with fasting insulin, HOMA-IR, triglycerides, and EFT. Levels were higher in insulin-resistant obese participants than in metabolically healthier obese individuals. ROC analysis showed good discriminative ability for insulin resistance (AUC=0.89) and moderate accuracy for identifying increased EFT (AUC=0.80). In multivariate analysis, BMI, but not sclerostin, remained an independent predictor of increased EFT. Conclusions Serum sclerostin is elevated in obese women and is associated with insulin resistance and adverse metabolic profiles. Although not independently associated with epicardial fat thickness, it reflects metabolic dysfunction related to visceral adiposity and may serve as an indicator of metabolically unhealthy obesity within this cohort.