August 25, 2005Diabetic Medicine
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
Key result
In non-diabetic men, non-alcoholic hepatic steatosis was associated with significantly higher plasma biomarkers of inflammation and endothelial dysfunction (P<0.01), largely mediated by visceral fat.
Why the study?
Are plasma biomarkers of inflammation and endothelial dysfunction increased in non-diabetic men with non-alcoholic hepatic steatosis, and is this mediated by visceral fat?
Population
100 non-smoking, healthy, non-diabetic male volunteers
Comparison
Non-alcoholic hepatic steatosis (HS) vs Without non-alcoholic hepatic steatosis
Design
Cross-sectional
Authors
Discussion
Loading...
Member takes
Implication
Association may reflect visceral fat mediation of endothelial dysfunction; hypothesis-generating, needs prospective studies before clinical relevance.
Key Points
- To assess whether increased plasma biomarkers of inflammation and endothelial dysfunction in non-diabetic men with non-alcoholic hepatic steatosis are mediated by visceral adipose tissue.
- Evaluated 100 non-smoking, healthy male volunteers categorized by presence (n=35) or absence (n=65) of non-alcoholic hepatic steatosis.
- Assessed hepatic steatosis and visceral fat via ultrasound and computed tomography, insulin resistance via HOMA, and plasma biomarkers including hs-CRP, fibrinogen, v-WF, and PAI-1 activity.
- Men with hepatic steatosis showed significantly higher plasma levels of hs-CRP, fibrinogen, v-WF, and PAI-1 activity than controls (all P < 0.01).
- Biomarker elevations remained significant after adjusting for age, BMI, blood pressure, insulin resistance, triglycerides, and liver enzymes, but were completely abolished after adjusting for visceral fat.
Study Design
Type
Cross-Sectional (n=100)
Structured PICO
Are plasma biomarkers of inflammation and endothelial dysfunction increased in non-diabetic men with non-alcoholic hepatic steatosis, and is this mediated by visceral fat?
P
Population
100 non-smoking, healthy, non-diabetic male volunteers evaluated for the relationship between non-alcoholic hepatic steatosis, visceral fat, and plasma biomarkers.
E
Exposure
Non-alcoholic hepatic steatosis (HS)
C
Comparator
Without non-alcoholic hepatic steatosis
O
Outcome
Plasma biomarkers of inflammation and endothelial dysfunction (hs-CRP, fibrinogen, von Willebrand factor, plasminogen activator inhibitor-1 activity)surrogate
Main Result
p-value: p=<0.01
Increased plasma biomarkers of inflammation and endothelial dysfunction in non-diabetic men with non-alcoholic hepatic steatosis are largely mediated by abdominal visceral fat accumulation.
Cite This Study
Targher et al. (2005) conducted a cross-sectional in Non-alcoholic hepatic steatosis (n=100). Non-alcoholic hepatic steatosis vs. Without non-alcoholic hepatic steatosis was evaluated on Plasma biomarkers of inflammation and endothelial dysfunction (hs-CRP, fibrinogen, v-WF, PAI-1 activity) (p=<0.01). In non-diabetic men, non-alcoholic hepatic steatosis was associated with significantly higher plasma biomarkers of inflammation and endothelial dysfunction (P<0.01), largely mediated by visceral fat.