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

Diabet Med. 2005 Oct;22(10):1354-8. doi: 10.1111/j.1464-5491.2005.01646.x.


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.

MeSH terms

  • Adipose Tissue / diagnostic imaging
  • Adipose Tissue / physiopathology*
  • Adult
  • Biomarkers / blood*
  • Blood Pressure / physiology
  • Body Mass Index
  • C-Reactive Protein / analysis
  • Cholesterol, HDL
  • Endothelium / physiopathology*
  • Fatty Liver / blood
  • Fatty Liver / diagnostic imaging
  • Fatty Liver / physiopathology*
  • Fibrinogen / analysis
  • Humans
  • Inflammation / blood
  • Inflammation / physiopathology*
  • Insulin Resistance / physiology
  • Male
  • Metabolic Syndrome / blood
  • Metabolic Syndrome / physiopathology
  • Plasminogen Activator Inhibitor 1 / analysis
  • Tomography, X-Ray Computed / methods
  • Triglycerides / blood
  • von Willebrand Factor / analysis


  • Biomarkers
  • Cholesterol, HDL
  • Plasminogen Activator Inhibitor 1
  • Triglycerides
  • von Willebrand Factor
  • Fibrinogen
  • C-Reactive Protein