Published online Aug 7, 2011. doi: 10.3748/wjg.v17.i29.3375
Revised: December 14, 2010
Accepted: December 21, 2010
Published online: August 7, 2011
Fatty liver is the most common cause of liver diseases in adults and children[1]. Fatty liver disease in humans is an insulin-resistant condition and the liver over-produces glucose and triglycerides due to impaired insulin action[2]. Fatty liver is an independent predictor of diabetes and cardiovascular disease[3]. There are three major sources for increased liver fat accumulation: excessive delivery of free fatty acids from lipolysis of superficial and visceral fat depots (60%), increased de novo hepatic lipogenesis (30%), and increased nutritional intake (10%)[4]. Recently, an increase in dietary cholesterol has been suggested to induce de novo fatty acid synthesis in hepatocytes via the LXRa-SREBP-1c pathway[5]. The most common cause of death in patients with non-alcoholic fatty liver disease (NAFLD) is coronary artery disease (CAD), and not chronic liver disease[6]. Fatty liver increases cardiovascular risk by classical (dyslipidemia, hypertension or diabetes) and by less conventional mechanisms. New emerging risk factors include leptin, adiponectin, pro-inflammatory cytokines such as interleukin-6, C-reactive protein and plasminogen activator inhibitor-1, which together lead to increased oxidative stress, lipotoxicity and endothelial dysfunction, which finally promote CAD[7]. When classical risk factors are superimposed on fatty liver accumulation, they may further increase the new metabolic risk factors, thus exacerbating CAD.
