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Review
. 2019 Feb 27;11(2):138-149.
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  1 , Christoffer A Hagemann  2 , Chunshan Wei  1 , Konstantin Kazankov  1 , Karen L Thomsen  1 , Filip K Knop  3 , Henning Grønbæk  4
Affiliations
Review

Bariatric surgery in patients with non-alcoholic fatty liver disease - from pathophysiology to clinical effects

Tea L Laursen et al. World J Hepatol. .

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

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Conflict of interest statement

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.

Figures

Figure 1
Figure 1
Risk factors and mechanisms associated with non-alcoholic fatty liver disease development and progression. NAFLD: Non-alcoholic fatty liver disease; NASH: Non-alcoholic steatohepatitis; ER: Endoplasmic reticulum; ROS: Reactive oxygen species; HCC: Hepatocellular carcinoma.
Figure 2
Figure 2
Main metabolic effects of bariatric surgery on remission. NAFLD: Non-alcoholic fatty liver disease.
See this image and copyright information in PMC

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