The biological mechanisms of accelerated atherosclerosis contributed by NAFLD are still poorly understood. NAFLD itself might act as a stimulus for further increased whole-body insulin resistance and dyslipidemia, PLX3397 concentration leading to accelerated atherosclerosis. Recent prospective studies demonstrated that raised liver enzymes independently predict the development of the MetS,28),29) implicating that patients with more severe fatty liver disease are

those who showed elevated liver Inhibitors,research,lifescience,medical function test results. Our result also showed that GTP was associated with carotid atherosclerosis, although the significance was disappeared after adjustment of other confounding factors. However, NAFLD was associated with increased carotid IMT independently classical risk factors and MetS, it is conceivable that other atherogenic mechanisms could be involved. One hypothesis could be a direct link between fatty liver and dyslipidemia,

endothelial dysfunction, Inhibitors,research,lifescience,medical or oxidative stress, and thus atherosclerosis.30) A strong association between NAFLD and endothelial dysfunction as measured by brachial artery flow mediated vasodilatation, a Inhibitors,research,lifescience,medical reliable marker of early atherosclerosis, was also recently described.31),32) Although the association between NAFLD and early or advanced carotid lesions is not new, we demonstrated this association for the first time in a random group of non-diabetic outpatients undergoing abdominal US for health screening. Despite several previous studies demonstrated the association between NAFLD and carotid IMT and/or carotid plaque, no general consensus exists

on the systematic screening of carotid atherosclerosis in patients with fatty liver disease. Our study suggests that an incidental finding of NAFLD was significantly associated with increased carotid Inhibitors,research,lifescience,medical IMT (≥ 1 mm) or plaque, which may represent a new Inhibitors,research,lifescience,medical indication for performing an assessment to search for silent arterial lesions. Thus, our findings might have important clinical and public health implications, emphasizing the importance of evaluating the CVD risk in patients diagnosed with NAFLD. Currently, it is not known whether improving NAFLD will ultimately prevent the development of CVD. In fact, the only general recommendation for management of NAFLD patients to date is related to lifestyle changes and an attempt at gradual weight loss along with appropriate Levetiracetam control of serum glucose and lipid levels.3),33) However, patients with NAFLD having increased carotid IMT could be candidates not only for aggressive treatment of the liver disease, but also for cholesterol lowering and aggressive treatment of underlying CVD risk factors; this would help to modify and potentially decrease the global CVD risk of these patients. Study limitations Because our study was cross-sectional, the causative nature of the associations cannot be established. Prospective studies will be required to sort out the time sequence of events.