Association of Biopsy-proven Nonalcoholic Fatty Liver Disease with Obesity and Apolipoproteins.

Abstract

Background and aims: Insulin resistance is considered the most important key mechanism in the development of nonalcoholic fatty liver disease (NAFLD). Some studies have reported that hyperinsulinemia decreases the hepatic secretion of apolipoprotein (Apo) B. Chronic hyperinsulinemia in NAFLD may be responsible for the accumulation of triglycerides in hepatocytes. We aimed to investigate whether apolipoproteins are related to histological findings in patients with biopsy-proven NAFLD. We also aimed to evaluate the effects of obesity on apolipoproteins and the pathogenesis of NAFLD.

Methods: In this cross-sectional study, 91 patients with biopsy-proven NAFLD were included. The control group consisted of 39 healthy subjects who had no history of liver disease or alcohol consumption and were matched for age, gender and smoking. Apoliprotein A1 and Apo B were measured via an immunoturbidimetric method with commercially available OSR6142 Apo A1 and OSR6143 Apo B immunoassay kits on an Olympus AU2700 analyzer.

Results: Age, gender, and smoking distribution were similar among nonalcoholic steatohepatitis patients, simple steatosis patients, and controls. The differences in the mean Apo A1 and Apo B levels and the Apo B/A1 ratio among non-alcoholic steatosis, simple steatosis, and control subjects did not reach statistical significance. In addition, patients with obese NAFLD had higher steatosis scores than patients with nonobese NAFLD (p<0.05).

Conclusions: Apo A1 and B levels and the B/A1 ratio were not associated with histopathological findings in patients with NAFLD. Fibrosis and ApoB1/A were found to be independent risk factors for metabolic associated fatty liver disease. In addition, obesity increases the grade of hepatic steatosis but does not cause lobular inflammation, ballooning or fibrosis.