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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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Sarcopenic Obesity, the Possible Culprit for Nonalcoholic Fatty Liver Disease or Fibrosis

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.

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 Gut and Liver, Song et al.4 investigated the relationship between the sarcopenic obesity status (sarcopenia alone, obesity alone, and sarcopenic obesity) and NAFLD or liver fibrosis in 2,191 participants included in a health check-up program. This study demonstrated that sarcopenic obesity was the risk factor for presence of NAFLD. Moreover, participants with sarcopenic obesity had the highest association with liver fibrosis in participants of other groups according to sarcopenia or obesity. In this editorial, several points could be discussed.

Firstly, sarcopenic obesity could be the confounding factor for metabolic risk abnormalities in terms of liver fibrosis. Previously, Park et al.5 have shown that the fibrotic burden was increased according to the number of metabolic risk abnormalities and/or diabetes in the participants in the health check-up cohort. Although Song et al.4 has adjusted for several metabolic components, but it would be worthwhile to adjust for the other components of the metabolic risk abnormalities (e.g. waist circumference, triglycerides, high-density lipoprotein) or the presence of metabolic syndrome as a whole.

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 et al.4 provided important evidence for this association, a cause-effect relationship cannot be accurately assessed in this study of cross-sectional observational design. In this regard, Sinn et al.10 recently conducted a longitudinal analysis to assess the impact of NAFLD on the loss of skeletal muscle mass in 52,815 participants who underwent at least two health check-up examinations with BIA. The 5-year loss of skeletal muscle mass was faster in participants with NAFLD (–281.3 g) than in those without NAFLD (–225.2 g). This suggests that NAFLD could be the risk factor for sarcopenia. However, an important concern remains that the characteristics of participants with and without NAFLD were quite different at baseline (i.e., lower SMI, sex, and comorbidity distribution).

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.

  1. Lee YH, Jung KS, Kim SU, et al. Sarcopaenia is associated with NAFLD independently of obesity and insulin resistance: Nationwide surveys (KNHANES 2008-2011). J Hepatol 2015;63:486-493.
    Pubmed CrossRef
  2. Koo BK, Kim D, Joo SK, et al. Sarcopenia is an independent risk factor for non-alcoholic steatohepatitis and significant fibrosis. J Hepatol 2017;66:123-131.
    Pubmed CrossRef
  3. Cruz-Jentoft AJ, Baeyens JP, Bauer JM, et al. Sarcopenia: European consensus on definition and diagnosis. Report of the European Working Group on Sarcopenia in Older People. Age Ageing 2010;39:412-423.
    Pubmed KoreaMed CrossRef
  4. Song W, Yoo SH, Jang J, et al. Association between sarcopenic obesity status and nonalcoholic fatty liver disease and fibrosis. Gut Liver 2023;17:130-138.
    Pubmed CrossRef
  5. Park H, Yoon EL, Kim M, et al. Selecting the target population for screening of hepatic fibrosis in primary care centers in Korea. J Clin Med 2022;11:1474.
    Pubmed KoreaMed CrossRef
  6. Jensen B, Braun W, Geisler C, et al. Limitations of fat-free mass for the assessment of muscle mass in obesity. Obes Facts 2019;12:307-315.
    Pubmed KoreaMed CrossRef
  7. Peng TC, Wu LW, Chen WL, Liaw FY, Chang YW, Kao TW. Nonalcoholic fatty liver disease and sarcopenia in a Western population (NHANES III): the importance of sarcopenia definition. Clin Nutr 2019;38:422-428.
    Pubmed CrossRef
  8. Kashiwagi K, Takayama M, Fukuhara K, et al. A significant association of non-obese non-alcoholic fatty liver disease with sarcopenic obesity. Clin Nutr ESPEN 2020;38:86-93.
    Pubmed CrossRef
  9. Bhanji RA, Narayanan P, Allen AM, Malhi H, Watt KD. Sarcopenia in hiding: the risk and consequence of underestimating muscle dysfunction in nonalcoholic steatohepatitis. Hepatology 2017;66:2055-2065.
    Pubmed CrossRef
  10. Sinn DH, Kang D, Kang M, et al. Nonalcoholic fatty liver disease and accelerated loss of skeletal muscle mass: a longitudinal cohort study. Hepatology 2022;76:1746-1754.
    Pubmed CrossRef

Article

Editorial

Gut and Liver 2023; 17(1): 8-9

Published online January 15, 2023 https://doi.org/10.5009/gnl220543

Copyright © Gut and Liver.

Sarcopenic Obesity, the Possible Culprit for Nonalcoholic Fatty Liver Disease or Fibrosis

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.

Body

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 Gut and Liver, Song et al.4 investigated the relationship between the sarcopenic obesity status (sarcopenia alone, obesity alone, and sarcopenic obesity) and NAFLD or liver fibrosis in 2,191 participants included in a health check-up program. This study demonstrated that sarcopenic obesity was the risk factor for presence of NAFLD. Moreover, participants with sarcopenic obesity had the highest association with liver fibrosis in participants of other groups according to sarcopenia or obesity. In this editorial, several points could be discussed.

Firstly, sarcopenic obesity could be the confounding factor for metabolic risk abnormalities in terms of liver fibrosis. Previously, Park et al.5 have shown that the fibrotic burden was increased according to the number of metabolic risk abnormalities and/or diabetes in the participants in the health check-up cohort. Although Song et al.4 has adjusted for several metabolic components, but it would be worthwhile to adjust for the other components of the metabolic risk abnormalities (e.g. waist circumference, triglycerides, high-density lipoprotein) or the presence of metabolic syndrome as a whole.

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 et al.4 provided important evidence for this association, a cause-effect relationship cannot be accurately assessed in this study of cross-sectional observational design. In this regard, Sinn et al.10 recently conducted a longitudinal analysis to assess the impact of NAFLD on the loss of skeletal muscle mass in 52,815 participants who underwent at least two health check-up examinations with BIA. The 5-year loss of skeletal muscle mass was faster in participants with NAFLD (–281.3 g) than in those without NAFLD (–225.2 g). This suggests that NAFLD could be the risk factor for sarcopenia. However, an important concern remains that the characteristics of participants with and without NAFLD were quite different at baseline (i.e., lower SMI, sex, and comorbidity distribution).

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.

CONFLICTS OF INTEREST

No potential conflict of interest relevant to this article was reported.

References

  1. Lee YH, Jung KS, Kim SU, et al. Sarcopaenia is associated with NAFLD independently of obesity and insulin resistance: Nationwide surveys (KNHANES 2008-2011). J Hepatol 2015;63:486-493.
    Pubmed CrossRef
  2. Koo BK, Kim D, Joo SK, et al. Sarcopenia is an independent risk factor for non-alcoholic steatohepatitis and significant fibrosis. J Hepatol 2017;66:123-131.
    Pubmed CrossRef
  3. Cruz-Jentoft AJ, Baeyens JP, Bauer JM, et al. Sarcopenia: European consensus on definition and diagnosis. Report of the European Working Group on Sarcopenia in Older People. Age Ageing 2010;39:412-423.
    Pubmed KoreaMed CrossRef
  4. Song W, Yoo SH, Jang J, et al. Association between sarcopenic obesity status and nonalcoholic fatty liver disease and fibrosis. Gut Liver 2023;17:130-138.
    Pubmed CrossRef
  5. Park H, Yoon EL, Kim M, et al. Selecting the target population for screening of hepatic fibrosis in primary care centers in Korea. J Clin Med 2022;11:1474.
    Pubmed KoreaMed CrossRef
  6. Jensen B, Braun W, Geisler C, et al. Limitations of fat-free mass for the assessment of muscle mass in obesity. Obes Facts 2019;12:307-315.
    Pubmed KoreaMed CrossRef
  7. Peng TC, Wu LW, Chen WL, Liaw FY, Chang YW, Kao TW. Nonalcoholic fatty liver disease and sarcopenia in a Western population (NHANES III): the importance of sarcopenia definition. Clin Nutr 2019;38:422-428.
    Pubmed CrossRef
  8. Kashiwagi K, Takayama M, Fukuhara K, et al. A significant association of non-obese non-alcoholic fatty liver disease with sarcopenic obesity. Clin Nutr ESPEN 2020;38:86-93.
    Pubmed CrossRef
  9. Bhanji RA, Narayanan P, Allen AM, Malhi H, Watt KD. Sarcopenia in hiding: the risk and consequence of underestimating muscle dysfunction in nonalcoholic steatohepatitis. Hepatology 2017;66:2055-2065.
    Pubmed CrossRef
  10. Sinn DH, Kang D, Kang M, et al. Nonalcoholic fatty liver disease and accelerated loss of skeletal muscle mass: a longitudinal cohort study. Hepatology 2022;76:1746-1754.
    Pubmed CrossRef
Gut and Liver

Vol.17 No.1
January, 2023

pISSN 1976-2283
eISSN 2005-1212

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