Influence of endotoxemy on development of non-alcoholic fatty liver disease

Abstract

Objective — to investigate endotoxin levels and to assess the relationship between endotoxemia and metabolic parameters and the degree of steatosis and fibrosis in patients with non‑alcoholic fatty liver disease (NAFLD) against the background of metabolic syndrome (MS).
 Materials and methods. The study included 68 patients with NAFLD with metabolic disorders and 20 people of the control group. Women prevailed in both investigational groups, the mean age was 49.34 ± 10.8 years. All patients underwent evaluation of their anthropometric parameters, investigation of body composition with determination of the percentage of visceral adipose tissue (VAT). To reveal VAT dysfunction, visceral adiposity index (VAI) was calculated with M. C. Amato method. Steatometry was performed by determining the wave attenuation coefficient and carrying out shear wave elastography. Endotoxin levels in blood serum were determined using a set of reagents «LAL Chromogenic Endpoint Assay» manufactured by «Hycult Biotech» (Netherlands).
 Results. Bacterial endotoxin levels in peripheral blood in the examined patients were almost three times higher in comparison with the control group (p < 0.05). Patients with overweight and obesity had significantly higher endotoxin levels compared with the control group (p < 0.05). The significant increase in endotoxin levels has been defined in obese NAFLD patients compared to the NAFLD patients with normal weight (p < 0.05). The direct correlation was found between endotoxin parameters and parameters of abdominal and visceral obesity. In the group of patients with high VAT activity, the maximal values of this indicator were observed, which significantly differed from the corresponding indicator in patients with low and medium VAI (p < 0.05). There was a direct correlation between moderate endotoxin and insulin resistance, a direct weak relationship between endotoxin and lipid profile parameters. In patients with grade 2 and 3 steatosis, significant differences in the level of endotoxemia were observed compared with the control group (p < 0.05) and patients with grade 1 steatosis (p < 0.05). At high grades of liver fibrosis (F3F4) there was a tendency to reduce endotoxemia compared with the low‑grade fibrosis (p < 0.05).
 Conclusions. The revealed relationships between endotoxemia level and metabolic factors of NAFLD development indicate the pathogenetic role of bacterial endotoxemia in triggering a cascade of metabolic reactions with the subsequent accumulation of lipids in the liver tissue and the progression of steatosis and fibrosis.