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World J Gastroenterol. Aug 7, 2011; 17(29): 3375-3376
Published online Aug 7, 2011. doi: 10.3748/wjg.v17.i29.3375
Nutritional recommendations for patients with non-alcoholic fatty liver diseases
Nimer Assy
Nimer Assy, Liver Unit, Ziv Medical Center, Safed 13100, Israel
Nimer Assy, Faculty of Medicine, Technion Institute, 32000 Haifa, Israel
Author contributions: Assy N wrote this paper.
Correspondence to: Nimer Assy, MD Head, Liver Unit Senior Lecturer, Faculty of Medicine, Haifa Technion Institute Ziv Medical Center POB 1008 Safed 13100, Israel. assy.n@ziv.health.gov.il
Telephone: +972-4-6828445 Fax: +972-4-6828442
Received: October 27, 2010
Revised: December 14, 2010
Accepted: December 21, 2010
Published online: August 7, 2011
Core Tip

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.