Insulin resistance and C-reactive protein as independent risk factors for non-alcoholic fatty liver disease in non-obese Asian men
Article first published online: 18 MAY 2004
Journal of Gastroenterology and Hepatology
Volume 19, Issue 6, pages 694–698, June 2004
How to Cite
PARK, S. H., KIM, B. I., YUN, J. W., KIM, J. W., PARK, D. I., CHO, Y. K., SUNG, I. K., PARK, C. Y., SOHN, C. I., JEON, W. K., KIM, H., RHEE, E. J., LEE, W. Y. and KIM, S. W. (2004), Insulin resistance and C-reactive protein as independent risk factors for non-alcoholic fatty liver disease in non-obese Asian men. Journal of Gastroenterology and Hepatology, 19: 694–698. doi: 10.1111/j.1440-1746.2004.03362.x
- Issue published online: 18 MAY 2004
- Article first published online: 18 MAY 2004
- Accepted for publication 20 October 2003.
- C-reactive protein;
- homeostasis model assessment;
- insulin resistance;
- non-alcoholic fatty liver disease
Background and Aim: Although insulin resistance is often considered the link between obesity and non-alcoholic fatty liver disease (NAFLD), the role of insulin resistance, independent of obesity, as a NAFLD risk factor in non-obese men has been less well established. Systemic inflammation may be accompanied by insulin resistance in healthy subjects. The goal of the present study was to examine if insulin resistance and systemic inflammatory markers are independent predictors of NAFLD in non-obese men.
Methods: The authors conducted a cross-sectional survey of 120 patients with NAFLD and 240 controls matched by age and body mass index. Controls had no evidence of alcohol abuse, hepatitis B or C, obesity, or previous history of diabetes, fasting hyperglycemia or hypertension. Diagnosis of NAFLD was based on an elevated alanine aminotransferase level and sonographic evidence of a fatty liver. Insulin resistance was determined using a homeostasis model assessment (HOMA-IR).
Results: The age-adjusted risk of developing NAFLD was strongly associated with the elevated levels in measurements of uric acid, fasting blood sugar, triglycerides, apolipoprotein B, C-reactive protein (CRP) and HOMA-IR, and decreased levels of high density lipoprotein cholesterol and apolipoprotein A-I. Multivariate analysis based on univariate analysis indicated that an increase in CRP (odds ratio [OR] = 1.37; 95% confidence interval [CI]: 1.06–1.77) per 1 SD (1.48 mg/L) and HOMA-IR (OR = 2.28; 95% CI: 1.67–3.11) per 1 SD (0.63) were independent risk factors for NAFLD.
Conclusion: Insulin resistance and systemic inflammatory response are of key importance for inducing NAFLD, particularly in apparently healthy non-obese men.