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Middle‐ and high‐molecular weight adiponectin levels in relation to nonalcoholic fatty liver disease

OBJECTIVE: Adiponectin (APN) circulates as high‐molecular weight (HMW), medium‐molecular weight (MMW), and low‐molecular weight (LMW) forms. Nonalcoholic fatty liver disease (NAFLD) is a common cause of chronic liver disease. Currently, the role of LMW, MMW, and HMW APN remains largely unclear in NA...

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Autores principales: Lian, Kun, Feng, Yu‐Nan, Li, Rong, Liu, Hao‐Lin, Han, Peng, Zhou, Lei, Li, Cheng‐Xiang, Wang, Qin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7171302/
https://www.ncbi.nlm.nih.gov/pubmed/31880002
http://dx.doi.org/10.1002/jcla.23148
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author Lian, Kun
Feng, Yu‐Nan
Li, Rong
Liu, Hao‐Lin
Han, Peng
Zhou, Lei
Li, Cheng‐Xiang
Wang, Qin
author_facet Lian, Kun
Feng, Yu‐Nan
Li, Rong
Liu, Hao‐Lin
Han, Peng
Zhou, Lei
Li, Cheng‐Xiang
Wang, Qin
author_sort Lian, Kun
collection PubMed
description OBJECTIVE: Adiponectin (APN) circulates as high‐molecular weight (HMW), medium‐molecular weight (MMW), and low‐molecular weight (LMW) forms. Nonalcoholic fatty liver disease (NAFLD) is a common cause of chronic liver disease. Currently, the role of LMW, MMW, and HMW APN remains largely unclear in NAFLD. METHODS: We examined the variation of these forms and analyzed the related clinical characteristics in NAFLD. A total of 63 male NAFLD patients (mean age: 43.00 ± 6.10 years) and 70 healthy male subjects (mean age: 42.53 ± 7.98 years) were included in the study. Total APN and other clinical characteristics were measured. The changes in HMW, MMW, and LMW APN were determined in NAFLD patients and NAFLD patients on a high‐fat diet, and the association between the groups was further analyzed. RESULTS: Decreased levels of total APN and three APN isoforms were found in NAFLD. Significantly decreased levels of HMW (P < .01) and MMW (P < .001) were observed in NAFLD of high‐fat diet patients. In NAFLD patients, height (R = −.270, P = .032) and N‐epsilon‐(carboxymethyl) lysine (R = −.259, P = .040) significantly correlated with total APN. HMW APN was significantly associated with fasting plasma glucose (R = .350, P = .016), alanine aminotransferase (R = −.321, P = .029), and aspartate aminotransferase (R = −.295, P = .045). Additionally, MMW APN was significantly associated with total cholesterol (R = .357, P = .014) and high‐density lipoprotein (R = .556, P < .0001). Low‐density lipoprotein (R = −.283, P = .054) was also clearly associated with LMW APN in NAFLD patients. CONCLUSION: These results suggest that HMW and MMW APN may be involved in the pathogenesis and progression of NAFLD.
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spelling pubmed-71713022020-04-21 Middle‐ and high‐molecular weight adiponectin levels in relation to nonalcoholic fatty liver disease Lian, Kun Feng, Yu‐Nan Li, Rong Liu, Hao‐Lin Han, Peng Zhou, Lei Li, Cheng‐Xiang Wang, Qin J Clin Lab Anal Research Articles OBJECTIVE: Adiponectin (APN) circulates as high‐molecular weight (HMW), medium‐molecular weight (MMW), and low‐molecular weight (LMW) forms. Nonalcoholic fatty liver disease (NAFLD) is a common cause of chronic liver disease. Currently, the role of LMW, MMW, and HMW APN remains largely unclear in NAFLD. METHODS: We examined the variation of these forms and analyzed the related clinical characteristics in NAFLD. A total of 63 male NAFLD patients (mean age: 43.00 ± 6.10 years) and 70 healthy male subjects (mean age: 42.53 ± 7.98 years) were included in the study. Total APN and other clinical characteristics were measured. The changes in HMW, MMW, and LMW APN were determined in NAFLD patients and NAFLD patients on a high‐fat diet, and the association between the groups was further analyzed. RESULTS: Decreased levels of total APN and three APN isoforms were found in NAFLD. Significantly decreased levels of HMW (P < .01) and MMW (P < .001) were observed in NAFLD of high‐fat diet patients. In NAFLD patients, height (R = −.270, P = .032) and N‐epsilon‐(carboxymethyl) lysine (R = −.259, P = .040) significantly correlated with total APN. HMW APN was significantly associated with fasting plasma glucose (R = .350, P = .016), alanine aminotransferase (R = −.321, P = .029), and aspartate aminotransferase (R = −.295, P = .045). Additionally, MMW APN was significantly associated with total cholesterol (R = .357, P = .014) and high‐density lipoprotein (R = .556, P < .0001). Low‐density lipoprotein (R = −.283, P = .054) was also clearly associated with LMW APN in NAFLD patients. CONCLUSION: These results suggest that HMW and MMW APN may be involved in the pathogenesis and progression of NAFLD. John Wiley and Sons Inc. 2019-12-27 /pmc/articles/PMC7171302/ /pubmed/31880002 http://dx.doi.org/10.1002/jcla.23148 Text en © 2019 The Authors. Journal of Clinical Laboratory Analysis Published by Wiley Periodicals, Inc. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Articles
Lian, Kun
Feng, Yu‐Nan
Li, Rong
Liu, Hao‐Lin
Han, Peng
Zhou, Lei
Li, Cheng‐Xiang
Wang, Qin
Middle‐ and high‐molecular weight adiponectin levels in relation to nonalcoholic fatty liver disease
title Middle‐ and high‐molecular weight adiponectin levels in relation to nonalcoholic fatty liver disease
title_full Middle‐ and high‐molecular weight adiponectin levels in relation to nonalcoholic fatty liver disease
title_fullStr Middle‐ and high‐molecular weight adiponectin levels in relation to nonalcoholic fatty liver disease
title_full_unstemmed Middle‐ and high‐molecular weight adiponectin levels in relation to nonalcoholic fatty liver disease
title_short Middle‐ and high‐molecular weight adiponectin levels in relation to nonalcoholic fatty liver disease
title_sort middle‐ and high‐molecular weight adiponectin levels in relation to nonalcoholic fatty liver disease
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7171302/
https://www.ncbi.nlm.nih.gov/pubmed/31880002
http://dx.doi.org/10.1002/jcla.23148
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