UNLABELLED: Recently the adipokin role in the pathogenesis of non-alcoholic fatty liver disease (NAFLD) has been suggested. The role of leptin and adiponectin is rather well known, however, there are only a few data concerning visfatin. THE AIM OF THE STUDY: To evaluate the serum level of visfatin in obese children with NAFLD. MATERIAL AND METHODS: Fasting serum level of visfatin was determined (ELISA) in 42 consecutive obese children (BMI >97 percentyla, aged 7-17 years, mean age 12 years) with suspected liver disease (hepatomegaly and/or elevation of transaminases and/or liver steatosis in ultrasound). Viral hepatitis, metabolic liver diseases and autoimmune hepatitis were excluded in all children. RESULTS: A fatty liver was confirmed in 30 children by ultrasonography; 16 of them also had increased ALT activity (NAFLD). Serum visfatin concentration in the examined group was significantly higher than in controls (n=20; p = 0.000085). Similarly, higher concentration of this adipokin was found in children with NAFLD than in controls (p = 0.0006). We also found a positive correlation between visfatin and IL-6 in children with NAFLD (r = 0.495; p = 0.05). There were no correlations between visfatin and anthropometric parameters, transaminases, lipids and HOMA-IR. CONCLUSION: The highest serum visfatin concentration in children with NAFLD and correlation between this adipokin and IL-6 suggests the role of visfatin in the development of liver inflammation in obese children with liver steatosis.
UNLABELLED: Recently the adipokin role in the pathogenesis of non-alcoholic fatty liver disease (NAFLD) has been suggested. The role of leptin and adiponectin is rather well known, however, there are only a few data concerning visfatin. THE AIM OF THE STUDY: To evaluate the serum level of visfatin in obesechildren with NAFLD. MATERIAL AND METHODS: Fasting serum level of visfatin was determined (ELISA) in 42 consecutive obesechildren (BMI >97 percentyla, aged 7-17 years, mean age 12 years) with suspected liver disease (hepatomegaly and/or elevation of transaminases and/or liver steatosis in ultrasound). Viral hepatitis, metabolic liver diseases and autoimmune hepatitis were excluded in all children. RESULTS: A fatty liver was confirmed in 30 children by ultrasonography; 16 of them also had increased ALT activity (NAFLD). Serum visfatin concentration in the examined group was significantly higher than in controls (n=20; p = 0.000085). Similarly, higher concentration of this adipokin was found in children with NAFLD than in controls (p = 0.0006). We also found a positive correlation between visfatin and IL-6 in children with NAFLD (r = 0.495; p = 0.05). There were no correlations between visfatin and anthropometric parameters, transaminases, lipids and HOMA-IR. CONCLUSION: The highest serum visfatin concentration in children with NAFLD and correlation between this adipokin and IL-6 suggests the role of visfatin in the development of liver inflammation in obesechildren with liver steatosis.