Non‐alcoholic hepatic steatosis and its relation to increased plasma biomarkers of inflammation and endothelial dysfunction in non‐diabetic men. Role of visceral adipose tissue

Abstract

Aims To compare plasma biomarkers of inflammation and endothelial dysfunction in individuals with and without non‐alcoholic hepatic steatosis (HS), and to evaluate whether such differences were mediated by the adverse metabolic pattern, typically found in these subjects. Methods HS (by ultrasound and computed tomography), visceral fat (by computed tomography), insulin resistance (by homeostasis model assessment—HOMA), plasma biomarkers of inflammation and endothelial dysfunction (hs‐C reactive protein, fibrinogen, von Willebrand factor, plasminogen activator inhibitor‐1 activity) were measured in 100 non‐smoking, healthy, male volunteers. Results Plasma hs‐CRP, fibrinogen, v‐WF and plasminogen activator inhibitor‐1 (PAI‐1) activity levels were markedly higher (P < 0.01 or less) in subjects with non‐alcoholic HS (n = 35) than in those without HS (n = 65). The former also had significantly higher values for body mass index (BMI), visceral fat, diastolic blood pressure, HOMA insulin resistance score, plasma insulin (both fasting and after glucose load), triglycerides, liver enzymes, and lower high‐density lipoprotein (HDL)‐cholesterol concentration. While the marked differences in these pro‐inflammatory biomarkers observed between the groups were little affected by adjustment for age, BMI, blood pressure values, HOMA insulin resistance score, plasma triglyceride and liver enzyme concentrations, they were completely abolished after controlling for visceral fat. Similarly, in multivariate regression analyses, increased visceral fat significantly predicted the pro‐inflammatory biomarkers, independently of HS and other potential confounders. Conclusions These results indicate that, in non‐smoking, non‐diabetic men, the significant increase of plasma biomarkers of inflammation and endothelial dysfunction in the presence of non‐alcoholic HS is largely mediated by abdominal visceral fat accumulation.