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Copyright ©The Author(s) 2019. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Hepatol. Feb 27, 2019; 11(2): 138-149
Published online Feb 27, 2019. doi: 10.4254/wjh.v11.i2.138
Bariatric surgery in patients with non-alcoholic fatty liver disease - from pathophysiology to clinical effects
Tea L Laursen, Christoffer A Hagemann, Chunshan Wei, Konstantin Kazankov, Karen L Thomsen, Filip K Knop, Henning Grønbæk
Tea L Laursen, Chunshan Wei, Konstantin Kazankov, Karen L Thomsen, Henning Grønbæk, Department of Hepatology and Gastroenterology, Aarhus University Hospital, Aarhus N DK-8200, Denmark
Christoffer A Hagemann, Gubra ApS, Hørsholm 2970, Denmark
Christoffer A Hagemann, Filip K Knop, Clinical Metabolic Physiology, Steno Diabetes Center Copenhagen, Gentofte Hospital, Hellerup 2900, Denmark
Christoffer A Hagemann, Filip K Knop, Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen 2200, Denmark
Chunshan Wei, Department of Hepatology, Shenzhen Traditional Chinese Medicine Hospital, the Fourth Clinical Medical College of Guangzhou University of Chinese Medicine, Shenzhen 518033, China
Filip K Knop, Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen 2200, Denmark
Author contributions: All authors contributed to the conception and design of this study, literature review and analysis, drafting, critical revision and editing, and approved the final version of this manuscript.
Conflict-of-interest statement: Christoffer A Hagemann is employed as an industrial PhD student in a joint venture between Gentofte Hospital, University of Copenhagen and the biotechnology company Gubra ApS. Filip K Knop has served on scientific advisory panels, been part of speaker’s bureaus for, served as a consultant to and/or received research support from Amgen, AstraZeneca, Boehringer Ingelheim, Carmot Therapeutics, Eli Lilly, Gubra, MedImmune, MSD/Merck, Norgine, Novo Nordisk, Sanofi, SNIPR Biome, and Zealand Pharma and is a minority shareholder of Antag Therapeutics. Henning Grønbæk received research grants from the Novo Nordisk Foundation, Abbvie, Intercept and is on the advisory board for Ipsen and Novartis. CW received a grant from the Sanming Project of Medicine in Shenzhen (SZSM201612074). The authors have no other financial disclosures or conflicts of interest to declare.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Corresponding author: Henning Grønbæk, MD, PhD, Professor, Department of Hepatology and Gastroenterology, Aarhus University Hospital, 99 Palle Juul-Jensens Boulevard, Entrance C, Level 1, C116, Aarhus N DK-8200, Denmark. henngroe@rm.dk
Telephone: +45-21-679281
Received: October 5, 2018
Peer-review started: October 6, 2018
First decision: October 26, 2018
Revised: November 1, 2018
Accepted: December 4, 2018
Article in press: December 5, 2018
Published online: February 27, 2019
Processing time: 145 Days and 3.6 Hours
Abstract

Non-alcoholic fatty liver disease (NAFLD) is increasingly recognized as a significant liver disease, and it covers the disease spectrum from simple steatosis with a risk of development of non-alcoholic steatohepatitis (NASH) to fibrosis, subsequent cirrhosis, end-stage liver failure, and liver cancer with a potential need for liver transplantation. NAFLD and NASH are closely related to obesity, metabolic syndrome, and type 2 diabetes (T2D). The role of gut hormones, especially glucagon-like peptide 1 (GLP-1), is important in NAFLD. Bariatric surgery has the potential for inducing great weight loss and may improve the symptoms of metabolic syndrome and T2D. Recent data demonstrated significant effects of bariatric surgery on GLP-1 and other gut hormones and important lipid metabolic and inflammatory abnormalities in the pathophysiology of NAFLD. Therefore, bariatric surgery may reverse the pathological liver changes in NAFLD and NASH patients. In the present review, we describe NAFLD and NASH pathophysiology and the primary effects of bariatric surgery on metabolic pathways. We performed a systematic review of the beneficial and harmful effects and focused on changes in liver disease severity in NAFLD and NASH patients. The specific focus was liver histopathology as assessed by the invasive liver biopsy. Additionally, we reviewed several non-invasive methods used for the assessment of liver disease severity following bariatric surgery.

Keywords: Non-alcoholic fatty liver disease; Non-alcoholic steatohepatitis; Bariatric surgery; Insulin resistance, Gut hormones; Glucagon-like peptide 1; Steatosis; Inflammation; Fibrosis

Core tip: Non-alcoholic fatty liver disease (NAFLD) is a significant liver disease with risks of steatohepatitis (NASH), fibrosis, and cirrhosis. NAFLD and NASH are closely related to obesity, the metabolic syndrome, and type 2 diabetes (T2D). Bariatric surgery induces weight loss and improves the features of the metabolic syndrome and T2D. Surgery may reverse pathological liver changes. In the present review, we focus on the primary effects of bariatric surgery on metabolic pathways and systematically reviews the effects of bariatric surgery on changes in liver disease severity in NAFLD and NASH patients.