Adipokine Profile in Non-alcoholic Fatty Liver Disease

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is commonly linked with metabolic disturbances such as central obesity, insulin resistance, dyslipidaemia and low-grade inflammation. Adipokines released from adipose tissue may influence hepatic fat accumulation, metabolic dysfunction and progression of liver injury. This study was conducted to assess the serum adipokine profile in patients with NAFLD, compare it with healthy controls and evaluate its relationship with anthropometric and biochemical parameters. MATERIALS AND METHODS: This case-control study included 100 participants, consisting of 50 patients with ultrasound-diagnosed NAFLD and 50 age- and sex-matched healthy controls. Demographic details, body mass index, waist circumference, fasting blood glucose, fasting insulin, lipid profile and liver function parameters were recorded. Serum adiponectin, leptin, resistin and visfatin levels were measured using enzyme-linked immunosorbent assay. Insulin resistance was assessed using the Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) index. The data were analysed to compare adipokine levels between the two groups and to determine their association with metabolic variables. RESULTS: The mean age of patients with NAFLD was 43.8 ± 9.6 years. Among them, 29 patients (58.0%) were males and 21 patients (42.0%) were females. Compared with controls, patients with NAFLD had significantly higher body mass index (29.1 ± 3.8 vs 23.7 ± 2.9 kg/m²), waist circumference (96.4 ± 8.7 vs 82.6 ± 7.9 cm), fasting blood glucose (112.8 ± 18.5 vs 91.6 ± 10.7 mg/dL), triglycerides (186.5 ± 42.3 vs 124.7 ± 31.8 mg/dL) and HOMA-IR (3.8 ± 1.2 vs 1.7 ± 0.6), with p < 0.001 for all comparisons. Serum adiponectin was significantly lower in the NAFLD group than in controls (5.9 ± 2.1 vs 10.8 ± 3.4 µg/mL; p < 0.001). In contrast, serum leptin (24.6 ± 8.9 vs 12.3 ± 5.4 ng/mL), resistin (14.8 ± 4.6 vs 8.7 ± 3.1 ng/mL) and visfatin (32.5 ± 10.2 vs 18.9 ± 7.6 ng/mL) were significantly higher among patients with NAFLD (p < 0.001). Adiponectin showed a negative correlation with body mass index, triglycerides and HOMA-IR, whereas leptin and resistin showed positive correlations with these parameters. CONCLUSION: Patients with NAFLD showed a clear adipokine imbalance, characterised by reduced adiponectin and increased leptin, resistin and visfatin levels. This pattern was associated with obesity, dyslipidaemia and insulin resistance, indicating that adipokine alterations may contribute to the metabolic and inflammatory mechanisms involved in NAFLD.