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World J Hepatol. Oct 27, 2013; 5(10): 550-557
Published online Oct 27, 2013. doi: 10.4254/wjh.v5.i10.550
Lipotoxicity in the liver
Veronika Zámbó, Laura Simon-Szabó, Péter Szelényi, Éva Kereszturi, Gábor Bánhegyi, Miklós Csala
Veronika Zámbó, Laura Simon-Szabó, Péter Szelényi, Éva Kereszturi, Gábor Bánhegyi, Miklós Csala, Department of Medical Chemistry, Molecular Biology and Pathobiochemistry, Semmelweis University, H-1444 Budapest, Hungary
Author contributions: Zámbó V prepared a structured overview of the recent literature and contributed to the writing of the manuscript; Simon-Szabó L, Szelényi P and Kereszturi É contributed to the data collection process; Bánhegyi G designed the aim of the editorial; Csala M generated the figures and wrote the manuscript.
Supported by Hungarian Scientific Research Fund (OTKA 104113 and 106060) and the Hungarian Research and Technological Innovation Fund (KMR_12-1-2012-0074)
Correspondence to: Gábor Bánhegyi, MD, PhD, Professor, Department of Medical Chemistry, Molecular Biology and Pathobiochemistry, Semmelweis University, Budapest, Tűzoltó u. 37-47, H-1444 Budapest, Hungary. banhegyi.gabor@med.semmelweis-univ.hu
Telephone: +36-1-2662615 Fax: +36-1-2663802
Received: August 13, 2013
Revised: September 27, 2013
Accepted: October 15, 2013
Published online: October 27, 2013
Core Tip

Core tip: Surplus of free fatty acids contributes to hepatic injuries in obesity and type 2 diabetes. Intracellular accumulation of fatty acyl-CoA causes oxidative and endoplasmic reticulum (ER) stress, which lead to cell death, inflammation and fibrosis. Steatohepatosis is the consequence of an intensive fat synthesis, aiming to reduce the metabolic burden. The higher toxicity of saturated vs unsaturated fatty acids is partly due to a limited capacity of the liver cells to insert them into triglycerides. Moreover, increased membrane saturation triggers the ER stress response though a unique mechanism, which aggravates the metabolic derangements and liver injuries.