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 liver disease worldwide. Patients with fatty liver disease die primarily from cardiovascular disease and not from chronic liver diseases. Hyperglycemia and hyperinsulinemia induce lipogenesis, thereby increasing the hepatic pool of fatty acids. This pool is also increased by increased delivery of fatty acids through the diet or lipolysis in adipose tissue. Nutritional consultations and lifestyle modification are important in the treatment of non-alcoholic fatty liver disease (NAFLD). Among the dietary constituents, combination of vitamin D, vitamin E, and omega-3 fatty acids shows promise for the treatment of NAFLD.
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.