Purpose: Adipocytokines may provide a link between metabolic syndrome, inflammation and cardiovascular disorder in non-alcoholic fatty liver disease (NAFLD) patients. We investigated whether NAFLD is associated with fat produced hormones and if this relation can affect the impaired endothelial structure and function.

Methods: We studied 34 patients (age 55 ± 13 years, 20M) with biopsy evidence of NAFLD, and 34 control subjects adjusted for classical risk factors. The changes in the diameter of the brachial artery were measured in response to reactive hyperemia and nitroglycerin. Mean IMT of common carotid arteries and carotid-femoral PWV were determined as markers of atherosclerosis and aortic stiffness respectively. Adipocytokines were measured by ELISA kit.

Results: NAFLD subjects had significantly reduced flow-mediated vasodilation (1.1 ± 1.9% vs 4.3± 3%, p<0.05), and mean value of carotid IMT (0.98 ± 0.3 vs 0.77 ± 0.2 mm, p<0.05) and PWV (8.4 ± 1.6 vs 7.3 ± 1.7 m/s, p<0.01) were increased compared to controls. NAFLD subjects had increased levels of leptin (21.81± ng/ml vs 12.12 ± 10 ng/ml, p<0.01), and resistin (5.174 ± 1.6 ng/ml vs 3.5 ± 1.28 ng/ml, p<0.01) and reduced levels of adiponectin (7.96 ± 5.19 μg/ml vs 13.17 ± 12.4 μg/ml, p<0.05) compared to controls. After adjustment for confounding factors, resistin levels were independently associated with impaired endothelial function (p<0.05, t=7.53, coefficient st=0.883) and leptin levels were independently associated with the increased mean IMT (p<0.01, t=6.92, coefficient st=0.888), and PWV (p< 0.05, t=2.258, coefficient st=0.32) in NAFLD patients.

Conclusion: Although the initiating events that trigger the development of atherosclerosis in NAFLD patients cannot be ascertained, the role of adipocytokines may identify a potential basis.