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Vol.17 No.1
January, 2023
Frequency : Bimonthly
pISSN 1976-2283
eISSN 2005-1212 
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
| Yong Chan Lee |
Professor of Medicine Director, Gastrointestinal Research Laboratory Veterans Affairs Medical Center, Univ. California San Francisco San Francisco, USA |
| 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 |
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.
The remaining articles are usually sent to two reviewers. It would be very helpful if you could suggest a selection of reviewers and include their contact details. We may not always use the reviewers you recommend, but suggesting reviewers will make our reviewer database much richer; in the end, everyone will benefit. We reserve the right to return manuscripts in which no reviewers are suggested.
The final responsibility for the decision to accept or reject lies with the editors. In many cases, papers may be rejected despite favorable reviews because of editorial policy or a lack of space. The editor retains the right to determine publication priorities, the style of the paper, and to request, if necessary, that the material submitted be shortened for publication.
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Seong Hee Kang1 
, Eileen L. Yoon2,3
Correspondence to: Eileen L. Yoon
ORCID https://orcid.org/0000-0003-0474-048X
E-mail mseileen80@hanyang.ac.kr
See See “Association between Sarcopenic Obesity Status and Nonalcoholic Fatty Liver Disease and Fibrosis” by Wolhwa Song, et al. on page 130, Vol. 17, No. 1, 2023
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 2023;17(1):8-9. https://doi.org/10.5009/gnl220543
Published online January 15, 2023, Published date January 15, 2023
Copyright © Gut and Liver.
Sarcopenia is a syndrome characterized by skeletal muscle loss associated with aging and is prevalent in chronic liver disease. Recent studies have reported that sarcopenia is a risk factor for the development of nonalcoholic fatty liver disease (NAFLD) and vice versa.1 Because sarcopenia and NAFLD share similar pathological mediators, such as insulin resistance, physical inactivity, and obesity, both disorders may have overlapping clinical presentations.2 This leads to the development of “sarcopenia obesity,” characterized by a lean body mass with preserved or increased fat mass.3
In this issue of
Firstly, sarcopenic obesity could be the confounding factor for metabolic risk abnormalities in terms of liver fibrosis. Previously, Park
Secondly, there is debate regarding the optimal techniques for the assessment of muscle mass in patients with NAFLD. Skeletal muscle index (SMI) assessed by bioimpedance analysis (BIA) has limitations, especially in patients with concomitant obesity, in whom it can overestimate the prevalence of sarcopenia.6 In general, SMI measured using BIA can be adjusted for both height (cm2) and weight (kg). This study used the SMI calculated by the ratio between the sum of the muscle mass values and body weight. Interestingly, a National Health and Nutrition Examination Survey III population study (n=2,551) showed that compared to healthy controls, participants with NAFLD were at a significantly higher risk of developing sarcopenia, based on the weight-adjusted SMI measured by BIA.7 However, the opposite was observed when sarcopenia was defined using height-adjusted SMI. In another study from Japan, they found that sarcopenic obesity was associated with non-obese NAFLD (body mass index <25 kg/m2) but not with obese NAFLD (body mass index ≥25 kg/m2) when they evaluated the presence of sarcopenia based on the measurement of bone densitometry, the gold standard diagnostic method for sarcopenia.8 These findings represent the limitations of BIA assessment in the diagnosis of sarcopenia in NAFLD and highlight the importance of standardizing diagnostic approaches.
Thirdly, it is difficult to determine a cause-effect relationship between NAFLD and sarcopenia as they share many complex interplaying mechanisms.2 For instance, NAFLD can lead to sarcopenia by activating myostatin, and low skeletal muscle mass can induce liver damage by activating the myostatin receptor in hepatic stellate cells.9 Although Song
In conclusion, identifying whether sarcopenia is a cause, consequence, or confounder of the metabolic risk abnormalities in the outcome of NAFLD or fibrosis remains a challenge. Nevertheless, this study demonstrated the important association of sarcopenic obesity status and increased the risk of developing NAFLD or liver fibrosis. The detailed factors of disease pathogenesis and accurate assessment method are yet to be elucidated.
No potential conflict of interest relevant to this article was reported.
Gut and Liver 2023; 17(1): 8-9
Published online January 15, 2023 https://doi.org/10.5009/gnl220543
Copyright © Gut and Liver.
Seong Hee Kang1 , Eileen L. Yoon2,3
1Department of Internal Medicine, Sanggye Paik Hospital, Inje University College of Medicine, Seoul, 2Department of Internal Medicine, Hanyang University Hospital, Hanyang University College of Medicine, and 3Hanyang Institute of Bioscience and Biotechnology, Hanyang University, Seoul, Korea
Correspondence to:Eileen L. Yoon
ORCID https://orcid.org/0000-0003-0474-048X
E-mail mseileen80@hanyang.ac.kr
See See “Association between Sarcopenic Obesity Status and Nonalcoholic Fatty Liver Disease and Fibrosis” by Wolhwa Song, et al. on page 130, Vol. 17, No. 1, 2023
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.
Sarcopenia is a syndrome characterized by skeletal muscle loss associated with aging and is prevalent in chronic liver disease. Recent studies have reported that sarcopenia is a risk factor for the development of nonalcoholic fatty liver disease (NAFLD) and vice versa.1 Because sarcopenia and NAFLD share similar pathological mediators, such as insulin resistance, physical inactivity, and obesity, both disorders may have overlapping clinical presentations.2 This leads to the development of “sarcopenia obesity,” characterized by a lean body mass with preserved or increased fat mass.3
In this issue of
Firstly, sarcopenic obesity could be the confounding factor for metabolic risk abnormalities in terms of liver fibrosis. Previously, Park
Secondly, there is debate regarding the optimal techniques for the assessment of muscle mass in patients with NAFLD. Skeletal muscle index (SMI) assessed by bioimpedance analysis (BIA) has limitations, especially in patients with concomitant obesity, in whom it can overestimate the prevalence of sarcopenia.6 In general, SMI measured using BIA can be adjusted for both height (cm2) and weight (kg). This study used the SMI calculated by the ratio between the sum of the muscle mass values and body weight. Interestingly, a National Health and Nutrition Examination Survey III population study (n=2,551) showed that compared to healthy controls, participants with NAFLD were at a significantly higher risk of developing sarcopenia, based on the weight-adjusted SMI measured by BIA.7 However, the opposite was observed when sarcopenia was defined using height-adjusted SMI. In another study from Japan, they found that sarcopenic obesity was associated with non-obese NAFLD (body mass index <25 kg/m2) but not with obese NAFLD (body mass index ≥25 kg/m2) when they evaluated the presence of sarcopenia based on the measurement of bone densitometry, the gold standard diagnostic method for sarcopenia.8 These findings represent the limitations of BIA assessment in the diagnosis of sarcopenia in NAFLD and highlight the importance of standardizing diagnostic approaches.
Thirdly, it is difficult to determine a cause-effect relationship between NAFLD and sarcopenia as they share many complex interplaying mechanisms.2 For instance, NAFLD can lead to sarcopenia by activating myostatin, and low skeletal muscle mass can induce liver damage by activating the myostatin receptor in hepatic stellate cells.9 Although Song
In conclusion, identifying whether sarcopenia is a cause, consequence, or confounder of the metabolic risk abnormalities in the outcome of NAFLD or fibrosis remains a challenge. Nevertheless, this study demonstrated the important association of sarcopenic obesity status and increased the risk of developing NAFLD or liver fibrosis. The detailed factors of disease pathogenesis and accurate assessment method are yet to be elucidated.
No potential conflict of interest relevant to this article was reported.
pISSN 1976-2283
eISSN 2005-1212
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
| Yong Chan Lee |
Professor of Medicine Director, Gastrointestinal Research Laboratory Veterans Affairs Medical Center, Univ. California San Francisco San Francisco, USA |
| 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 |
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.
The remaining articles are usually sent to two reviewers. It would be very helpful if you could suggest a selection of reviewers and include their contact details. We may not always use the reviewers you recommend, but suggesting reviewers will make our reviewer database much richer; in the end, everyone will benefit. We reserve the right to return manuscripts in which no reviewers are suggested.
The final responsibility for the decision to accept or reject lies with the editors. In many cases, papers may be rejected despite favorable reviews because of editorial policy or a lack of space. The editor retains the right to determine publication priorities, the style of the paper, and to request, if necessary, that the material submitted be shortened for publication.
