©The Author(s) 2021. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jan 7, 2021; 27(1): 1-18
Published online Jan 7, 2021. doi: 10.3748/wjg.v27.i1.1
Published online Jan 7, 2021. doi: 10.3748/wjg.v27.i1.1
Experimental models of metabolic and alcoholic fatty liver disease
Delfin Gerard Buyco, Jasmin Martin, Sookyoung Jeon, Royce Hooks, Chelsea Lin, Rotonya Carr, Division of Gastroenterology, University of Pennsylvania, Philadelphia, PA 19104, United States
Author contributions: Buyco DG wrote the first draft of the paper; Buyco DG, Martin J, Jeon S, Hooks R, Lin C and Carr RM performed the research for the manuscript and edited all drafts of the paper.
Conflict-of-interest statement: The authors report no conflicts of interest.
Corresponding author: Rotonya Carr, MD, Assistant Professor, Division of Gastroenterology, University of Pennsylvania, 421 Curie Boulevard 907 Biomedical Research Center, Philadelphia, PA 19104, United States. rotonya.carr@pennmedicine.upenn.edu
Received: September 3, 2020
Peer-review started: September 3, 2020
First decision: October 17, 2020
Revised: November 1, 2020
Accepted: December 6, 2020
Article in press: December 6, 2020
Published online: January 7, 2021
Processing time: 114 Days and 18.8 Hours
Peer-review started: September 3, 2020
First decision: October 17, 2020
Revised: November 1, 2020
Accepted: December 6, 2020
Article in press: December 6, 2020
Published online: January 7, 2021
Processing time: 114 Days and 18.8 Hours
Core Tip
Core Tip: Experimental animal and cell culture models have been developed to study the “syndrome of metabolic and alcoholic steatohepatitis” (SMASH), in which concomitant non-alcoholic fatty liver disease and alcoholic liver disease risk factors play a role in liver injury. These models demonstrate that obesity, metabolic syndrome, and alcohol consumption synergistically contribute to lipid dysregulation, oxidative stress, inflammation, and fibrogenesis. The pathogenesis of SMASH in these experimental models is dependent on obesogenic diet composition, alcohol consumption patterns, alcohol dosage, and genetic background.