Aim: Resistin and adiponectin are recently discovered protein hormones, which are produced and secreted by adipocytes. Nonalcoholic fatty liver disease (NAFLD) is a metabolic syndrome, which is associated with obesity. The aim of this study was to evaluate the changes of serum adiponectin and resistin in patients with NAFLD and to determine the relationship between serum adipokine levels and clinicopathologic parameters of NAFLD.
Methods: Forty-three patients with NAFLD and 43 controls were enrolled in this pair-matched study. Body weight, height, body mass index, abdominal wall fat thickness, waist circumference, hip circumference, and the percentage of body fat were measured. Additionally, serum lipid, glucose, alanine aminotransferase, aspartate aminotransferase, adiponectin, and resistin were determined in all individuals. Serum adiponectin and resistin levels were determined using ELISA kits.
Results: Serum adiponectin levels were significantly lower in patients with NAFLD compared to the control group (control: 2.01+/-1.10 mg/l vs. NAFLD: 1.38+/-0.65 mg/l, P<0.01). Serum resistin levels were significantly elevated in patients with NAFLD compared to the control group (control: 4.70+/-3.30 ng/ml vs. NAFLD: 9.20+/-7.20 ng/ml, P<0.05). Serum adiponectin concentration was negatively correlated with the waist circumference (rho=-0.425), body mass index (rho=-0.329), percentage of body fat (rho=-0.256), abdominal wall fat thickness (rho=-0.226), and fasting blood glucose concentration (rho=-0.242), but was positively correlated with HDL (rho=0.226). Serum resistin concentration was positively correlated with waist circumference (rho=0.237). No correlation was found between resistin levels and blood pressure, fasting blood glucose concentration, triglyceride, total cholesterol, and HDL.
Conclusion: NAFLD patients had lower adiponectin levels and higher resistin levels. A positive correlation was found between resistin and waist circumference, whereas a negative correlation was found between adiponectin and waist circumference, body mass index, percentage of body fat, abdominal wall fat thickness, and fasting blood glucose concentration. These data suggested that hypoadiponectinemia and hyperresistinemia might be involved in the development of NAFLD.