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  • 1. Aims and Scope

    Gut and Liver is an international journal of gastroenterology, focusing on the gastrointestinal tract, liver, biliary tree, pancreas, motility, and neurogastroenterology. Gut atnd Liver delivers up-to-date, authoritative papers on both clinical and research-based topics in gastroenterology. The Journal publishes original articles, case reports, brief communications, letters to the editor and invited review articles in the field of gastroenterology. The Journal is operated by internationally renowned editorial boards and designed to provide a global opportunity to promote academic developments in the field of gastroenterology and hepatology. +MORE

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    Yong Chan Lee Professor of Medicine
    Director, Gastrointestinal Research Laboratory
    Veterans Affairs Medical Center, Univ. California San Francisco
    San Francisco, USA

    Deputy Editor

    Deputy Editor
    Jong Pil Im Seoul National University College of Medicine, Seoul, Korea
    Robert S. Bresalier University of Texas M. D. Anderson Cancer Center, Houston, USA
    Steven H. Itzkowitz Mount Sinai Medical Center, NY, USA
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    All papers submitted to Gut and Liver are reviewed by the editorial team before being sent out for an external peer review to rule out papers that have low priority, insufficient originality, scientific flaws, or the absence of a message of importance to the readers of the Journal. A decision about these papers will usually be made within two or three weeks.
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Impact of Evolutionary Changes in Nonalcoholic Fatty Liver Disease on Lung Function Decline

Hyun Woo Lee1 , Goh Eun Chung2 , Bo Kyung Koo3 , Hyungtai Sim4 , Murim Choi4 , Dong Hyeon Lee5 , Seung Ho Choi2 , Soo Heon Kwak6 , Deog Kyeom Kim1,7 , and Won Kim5,7 , on behalf of the Innovative Target Exploration of NAFLD (ITEN) consortium

1Division of Respiratory and Critical Care, Department of Internal Medicine, Seoul Metropolitan Government Seoul National University Boramae Medical Center, 2Department of Internal Medicine, Healthcare System Gangnam Center, Seoul National University Hospital, 3Division of Endocrinology, Department of Internal Medicine, Seoul Metropolitan Government Seoul National University Boramae Medical Center, 4Department of Biomedical Sciences, Seoul National University College of Medicine, 5Division of Gastroenterology and Hepatology, Department of Internal Medicine, Seoul Metropolitan Government Seoul National University Boramae Medical Center, 6Department of Internal Medicine, Seoul National University Hospital, and 7Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea

Correspondence to:Deog Kyeom Kim
ORCID https://orcid.org/0000-0001-9379-8098
E-mail kimdkmd@snu.ac.kr

Won Kim
ORCID https://orcid.org/0000-0002-2926-1007
E-mail drwon1@snu.ac.kr

Hyun Woo Lee and Goh Eun Chung contributed equally to this work as first authors.

Received: November 26, 2021; Revised: February 23, 2022; Accepted: February 24, 2022

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Gut Liver

Published online May 25, 2022

Copyright © Gut and Liver.

Abstract

Background/Aims: A relationship between fatty liver and lung function impairment has been identified, and both are independently associated with metabolic dysfunction. However, the temporal relationship between changes in fatty liver status and lung function and their genome-wide association remain unclear.
Methods: This longitudinal cohort consisted of subjects who received serial health check-ups, including liver ultrasonography and spirometry, for ≥3 years between 2003 and 2015. Lung function decline rates were classified as “slow” and “accelerated” and compared among four different sonographic changes in steatosis status: “normal,” “improved,” “worsened,” and “persistent.” A genome-wide association study was conducted between the two groups: normal/improved steatosis with a slow decline in lung function versus worsened/persistent steatosis with an accelerated decline in lung function.
Results: Among 6,149 individuals, the annual rates of decline in forced vital capacity (FVC) and forced expiratory volume measured in the first second of exhalation (FEV1) were higher in the worsened/persistent steatosis group than in the normal/improved steatosis group. In multivariable analysis, persistent or worsened status of fatty liver was significantly associated with accelerated declines in FVC (persistent status, odds ratio [OR]=1.22, 95% confidence interval [CI]=1.04–1.44; worsened status, OR=1.30, 95% CI=1.12–1.50), while improved status of fatty liver was significantly associated with slow declines in FEV1 (OR=0.77, 95% CI=0.64–0.92). The PNPLA3 risk gene was most strongly associated with steatosis status change and accelerated declines in FVC (rs12483959, p=2.61×10-7) and FEV1 (rs2294433, p=3.69×10-8).
Conclusions: Regression of fatty liver is related to lung function decline. Continuing efforts to improve fatty liver may preserve lung function, especially for subjects with a high genetic risk.

Keywords: Non-alcoholic fatty liver disease, Disease progression, Pulmonary function test, Genome-wide association study, Longitudinal study


Article

ahead

Gut and Liver

Published online May 25, 2022

Copyright © Gut and Liver.

Impact of Evolutionary Changes in Nonalcoholic Fatty Liver Disease on Lung Function Decline

Hyun Woo Lee1 , Goh Eun Chung2 , Bo Kyung Koo3 , Hyungtai Sim4 , Murim Choi4 , Dong Hyeon Lee5 , Seung Ho Choi2 , Soo Heon Kwak6 , Deog Kyeom Kim1,7 , and Won Kim5,7 , on behalf of the Innovative Target Exploration of NAFLD (ITEN) consortium

1Division of Respiratory and Critical Care, Department of Internal Medicine, Seoul Metropolitan Government Seoul National University Boramae Medical Center, 2Department of Internal Medicine, Healthcare System Gangnam Center, Seoul National University Hospital, 3Division of Endocrinology, Department of Internal Medicine, Seoul Metropolitan Government Seoul National University Boramae Medical Center, 4Department of Biomedical Sciences, Seoul National University College of Medicine, 5Division of Gastroenterology and Hepatology, Department of Internal Medicine, Seoul Metropolitan Government Seoul National University Boramae Medical Center, 6Department of Internal Medicine, Seoul National University Hospital, and 7Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea

Correspondence to:Deog Kyeom Kim
ORCID https://orcid.org/0000-0001-9379-8098
E-mail kimdkmd@snu.ac.kr

Won Kim
ORCID https://orcid.org/0000-0002-2926-1007
E-mail drwon1@snu.ac.kr

Hyun Woo Lee and Goh Eun Chung contributed equally to this work as first authors.

Received: November 26, 2021; Revised: February 23, 2022; Accepted: February 24, 2022

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Background/Aims: A relationship between fatty liver and lung function impairment has been identified, and both are independently associated with metabolic dysfunction. However, the temporal relationship between changes in fatty liver status and lung function and their genome-wide association remain unclear.
Methods: This longitudinal cohort consisted of subjects who received serial health check-ups, including liver ultrasonography and spirometry, for ≥3 years between 2003 and 2015. Lung function decline rates were classified as “slow” and “accelerated” and compared among four different sonographic changes in steatosis status: “normal,” “improved,” “worsened,” and “persistent.” A genome-wide association study was conducted between the two groups: normal/improved steatosis with a slow decline in lung function versus worsened/persistent steatosis with an accelerated decline in lung function.
Results: Among 6,149 individuals, the annual rates of decline in forced vital capacity (FVC) and forced expiratory volume measured in the first second of exhalation (FEV1) were higher in the worsened/persistent steatosis group than in the normal/improved steatosis group. In multivariable analysis, persistent or worsened status of fatty liver was significantly associated with accelerated declines in FVC (persistent status, odds ratio [OR]=1.22, 95% confidence interval [CI]=1.04–1.44; worsened status, OR=1.30, 95% CI=1.12–1.50), while improved status of fatty liver was significantly associated with slow declines in FEV1 (OR=0.77, 95% CI=0.64–0.92). The PNPLA3 risk gene was most strongly associated with steatosis status change and accelerated declines in FVC (rs12483959, p=2.61×10-7) and FEV1 (rs2294433, p=3.69×10-8).
Conclusions: Regression of fatty liver is related to lung function decline. Continuing efforts to improve fatty liver may preserve lung function, especially for subjects with a high genetic risk.

Keywords: Non-alcoholic fatty liver disease, Disease progression, Pulmonary function test, Genome-wide association study, Longitudinal study

Gut and Liver

Vol.16 No.3
May, 2022

pISSN 1976-2283
eISSN 2005-1212

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