*Laura Martinez-Gili,1,2 Carmen Garcia-Ruiz,1-3 Carlos Fernandez-Checa1-3
1. Department of Cell Death and Proliferation, Institute of Biomedical Research of Barcelona (IIBB), CSIC, Barcelona, Spain
2. Liver Unit, Hospital Clinic i Provincial de Barcelona, IDIBAPS and CIBERehd, Barcelona, Spain
3. Research Center for ALPD, Keck School of Medicine, University of Southern California, Los Angeles, California, USA
*Correspondence to firstname.lastname@example.org
Disclosure: The authors have declared no conflicts of interest.
Received: 18.03.16 Accepted: 04.05.16
Citation: EMJ Hepatol. 2016;4:76-83.
The role of different lipid species such as free fatty acids and sphingolipids in non-alcoholic fatty liver disease (NAFLD) has been extensively studied during the last decade. In addition, free cholesterol accumulation in hepatocytes plays a crucial role in the transition from steatosis to steatohepatitis. However, the contribution of these lipids to NAFLD pathology is often evaluated individually. This review attempts to enclose the main metabolic and signalling connections between lipotoxic lipid species, and how their homeostasis is disrupted in NAFLD.