Increase in the skeletal muscle mass to body fat mass ratio predicts the decline in transaminase in patients with nonalcoholic fatty liver disease.
Adipose Tissue
Adolescent
Adult
Aged
Aged, 80 and over
Alanine Transaminase
/ blood
Aspartate Aminotransferases
/ blood
Body Composition
/ physiology
Electric Impedance
Female
Humans
Male
Middle Aged
Muscle, Skeletal
Non-alcoholic Fatty Liver Disease
/ enzymology
Retrospective Studies
Transaminases
/ blood
Young Adult
gamma-Glutamyltransferase
/ blood
Body fat mass
NAFLD
SF ratio
SMI
Journal
Journal of gastroenterology
ISSN: 1435-5922
Titre abrégé: J Gastroenterol
Pays: Japan
ID NLM: 9430794
Informations de publication
Date de publication:
Feb 2019
Feb 2019
Historique:
received:
24
04
2018
accepted:
11
06
2018
pubmed:
28
6
2018
medline:
17
3
2020
entrez:
28
6
2018
Statut:
ppublish
Résumé
The aim of this retrospective study was to determine the effect of skeletal muscle and body fat on liver function in patients with nonalcoholic fatty liver disease (NAFLD) diagnosed by liver biopsy. Among the 219 patients with NAFLD enrolled in this study was a cohort of 139 patients who had their body composition measured with Inbody720 at baseline and at ≥ 1 year postbaseline, to elucidate the relationship between liver function and changes in skeletal muscle and body fat mass. Multivariate analysis was used to identify factors influencing low skeletal muscle mass index (SMI, defined as 7 kg/m Of the 219 patients enrolled, 27 (12.3%) had a low SMI. Patient age (> 70 years) and female gender were identified as risk factors for low SMI. Hepatic fibrosis was not associated with SMI. In the cohort followed up at baseline and 12 months later, transaminase activity, body fat mass, and SMI significantly decreased over time. Changes in the SF ratio were significantly associated with changes in liver function. An increase in the SF ratio [hazard ratio (HR) 10.99 in men, 6.849 in women] was a predictor of reduced ALT, independent of age and other backgrounds. In the patients with NAFLD, SMI was decreased, even in the early stages of NAFLD. Therapeutic strategies for NAFLD require a reduction in body fat mass and the maintenance of skeletal muscle is also needed.
Sections du résumé
BACKGROUND
BACKGROUND
The aim of this retrospective study was to determine the effect of skeletal muscle and body fat on liver function in patients with nonalcoholic fatty liver disease (NAFLD) diagnosed by liver biopsy.
METHODS
METHODS
Among the 219 patients with NAFLD enrolled in this study was a cohort of 139 patients who had their body composition measured with Inbody720 at baseline and at ≥ 1 year postbaseline, to elucidate the relationship between liver function and changes in skeletal muscle and body fat mass. Multivariate analysis was used to identify factors influencing low skeletal muscle mass index (SMI, defined as 7 kg/m
RESULTS
RESULTS
Of the 219 patients enrolled, 27 (12.3%) had a low SMI. Patient age (> 70 years) and female gender were identified as risk factors for low SMI. Hepatic fibrosis was not associated with SMI. In the cohort followed up at baseline and 12 months later, transaminase activity, body fat mass, and SMI significantly decreased over time. Changes in the SF ratio were significantly associated with changes in liver function. An increase in the SF ratio [hazard ratio (HR) 10.99 in men, 6.849 in women] was a predictor of reduced ALT, independent of age and other backgrounds.
CONCLUSIONS
CONCLUSIONS
In the patients with NAFLD, SMI was decreased, even in the early stages of NAFLD. Therapeutic strategies for NAFLD require a reduction in body fat mass and the maintenance of skeletal muscle is also needed.
Identifiants
pubmed: 29948305
doi: 10.1007/s00535-018-1485-8
pii: 10.1007/s00535-018-1485-8
doi:
Substances chimiques
gamma-Glutamyltransferase
EC 2.3.2.2
Transaminases
EC 2.6.1.-
Aspartate Aminotransferases
EC 2.6.1.1
Alanine Transaminase
EC 2.6.1.2
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
160-170Commentaires et corrections
Type : CommentIn
Type : CommentIn
Références
Gastroenterology. 1999 Jun;116(6):1413-9
pubmed: 10348825
Am J Gastroenterol. 1999 Sep;94(9):2467-74
pubmed: 10484010
Diabetes Care. 1999 Nov;22(11):1808-12
pubmed: 10546012
Eur J Clin Nutr. 2001 Aug;55(8):663-72
pubmed: 11477465
J Clin Endocrinol Metab. 2003 Dec;88(12):5766-72
pubmed: 14671166
J Am Geriatr Soc. 2003 Nov;51(11):1533-8
pubmed: 14687381
Lancet. 2004 Jan 10;363(9403):157-63
pubmed: 14726171
Hepatology. 2005 Jun;41(6):1313-21
pubmed: 15915461
Am J Clin Nutr. 2005 Aug;82(2):428-34
pubmed: 16087989
Lancet. 2005 Sep 24-30;366(9491):1059-62
pubmed: 16182882
Lancet. 2005 Nov 5;366(9497):1640-9
pubmed: 16271645
J Appl Physiol (1985). 2007 Mar;102(3):919-25
pubmed: 17095641
J Gastroenterol Hepatol. 2007 Jun;22(6):775-7
pubmed: 17565629
Adv Physiol Educ. 2008 Jun;32(2):120-6
pubmed: 18539850
Appl Physiol Nutr Metab. 2009 Jun;34(3):396-402
pubmed: 19448705
Clin Gastroenterol Hepatol. 2010 Nov;8(11):979-85
pubmed: 20621200
Maturitas. 2011 Apr;68(4):331-6
pubmed: 21353405
Clin Gastroenterol Hepatol. 2012 Feb;10(2):166-73, 173.e1
pubmed: 21893129
PLoS One. 2011;6(9):e24633
pubmed: 21931785
Eur J Gastroenterol Hepatol. 2011 Nov;23(11):982-9
pubmed: 21971339
J Lipid Res. 2012 May;53(5):990-9
pubmed: 22394502
Hepatology. 2012 Jun;55(6):2005-23
pubmed: 22488764
J Gastrointestin Liver Dis. 2012 Jun;21(2):205-8
pubmed: 22720311
Clin Nutr. 2012 Oct;31(5):583-601
pubmed: 22809635
Hepatol Res. 2013 Feb;43(2):106-12
pubmed: 23409849
J Am Coll Cardiol. 2013 Sep 3;62(10):921-5
pubmed: 23850922
Clin Nutr. 2014 Oct;33(5):900-5
pubmed: 24140234
J Clin Gastroenterol. 2015 Sep;49(8):690-6
pubmed: 25291348
Biogerontology. 2015 Feb;16(1):15-29
pubmed: 25376109
J Hepatol. 2015 Jul;63(1):131-40
pubmed: 25724366
Hepatol Res. 2015 Apr;45(4):363-77
pubmed: 25832328
Maturitas. 2015 Sep;82(1):56-64
pubmed: 25882761
Hepatol Res. 2016 Jul;46(8):743-51
pubmed: 26579878
Hepatology. 2016 Mar;63(3):776-86
pubmed: 26638128
Hepatology. 2016 Jul;64(1):73-84
pubmed: 26707365
Nutrients. 2016 Mar 29;8(4):189
pubmed: 27043617
Hepatol Res. 2016 Sep;46(10):951-63
pubmed: 27481650
Clin Gastroenterol Hepatol. 2017 Jan;15(1):96-102.e3
pubmed: 27521509
J Hepatol. 2017 Jan;66(1):123-131
pubmed: 27599824
J Hepatol. 2017 Jan;66(1):142-152
pubmed: 27639843
Endocr J. 2017 Mar 31;64(3):269-281
pubmed: 27916783
J Gastroenterol. 2018 Apr;53(4):535-547
pubmed: 28791501