Circulating Adropin and Preptin In Non-Alcoholic Steatohepatitis and Their Relationship with Carotid Intima Media Thickness

Background Adropin and preptin are recently identified as peptide hormones that act as potential mediators between metabolic dysfunction and vascular injury. However, their clinical relevance in non-alcoholic steatohepatitis (NASH) remains unclear. Thus, we aimed to evaluate serum adropin and preptin levels and their association with carotid intima-media thickness (CIMT) in patients with biopsy-proven NASH. Methods This cross-sectional study included 40 patients with histologically proven NASH and 30 age- and sex-matched healthy controls. This study enrolled 40 NASH patients and 30 healthy controls. None of the participants had diabetes, hypertension, or hyperlipidemia. Anthropometric, biochemical measurements and doppler ultrasonography were performed. Results Serum adropin and preptin levels were significantly lower in NASH patients compared to controls (p = 0.02 and p = 0.03, respectively). Adropin levels were significantly negatively correlated with body mass index (BMI), body fat mass (BFM), body fat percentage (BFP), and HOMA-IR (all p < 0.05). In contrast, preptin levels showed no significant correlation with BMI, BFM, or BFP, and demonstrated a non-significant positive association with HOMA-IR. CIMT was significantly higher in NASH patients (0.63 ± 0.09 mm vs. 0.49 ± 0.06 mm; p < 0.01), and positively correlated with BMI and LDL, but not with adropin, preptin, or HOMA-IR. Furthermore, both peptides exhibited moderate negative correlations with steatosis grade and necroinflammatory activity (p < 0.05), but they showed weak, non-significant negative correlations with fibrosis (p = 0.08). In multivariate analysis, only BMI was independently associated with NASH (OR = 1.44, 95% CI: 1.13–1.84, p = 0.004). Conclusion Reduced adropin and preptin levels in NASH patients were associated with metabolic and histological severity, independent of vascular changes. These peptides may serve as potential biomarkers for disease activity in NASH. But, further studies are needed to their clinical utility as biomarkers or therapeutic targets in NASH.