Cargando…

HbA1c may contribute to the development of non-alcoholic fatty liver disease even at normal-range levels

Previous clinical studies highlighted nonalcoholic fatty liver disease (NAFLD) as a hepatic facet of metabolic syndrome, which progresses toward Type 2 diabetes along with an elevation of HbA1c in the blood. Longitudinal observations were performed in a cohort of 2811 participants with no liver dise...

Descripción completa

Detalles Bibliográficos
Autores principales: Chen, Changxi, Zhu, Zhongwei, Mao, Yushan, Xu, Yimin, Du, Juan, Tang, Xiaoping, Cao, Hongbao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Portland Press Ltd. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6997109/
https://www.ncbi.nlm.nih.gov/pubmed/31940026
http://dx.doi.org/10.1042/BSR20193996
_version_ 1783493624107892736
author Chen, Changxi
Zhu, Zhongwei
Mao, Yushan
Xu, Yimin
Du, Juan
Tang, Xiaoping
Cao, Hongbao
author_facet Chen, Changxi
Zhu, Zhongwei
Mao, Yushan
Xu, Yimin
Du, Juan
Tang, Xiaoping
Cao, Hongbao
author_sort Chen, Changxi
collection PubMed
description Previous clinical studies highlighted nonalcoholic fatty liver disease (NAFLD) as a hepatic facet of metabolic syndrome, which progresses toward Type 2 diabetes along with an elevation of HbA1c in the blood. Longitudinal observations were performed in a cohort of 2811 participants with no liver disease at inception. The rate of the conversion into NAFLD was 15.7% (440/2811), with a steady increase in prevalence observed in sub-cohorts with increasing HbA1c levels. Moreover, regression analysis indicated that HbA1c levels serve as the risk factors for NAFLD after multiple adjustments (odds ratio: 1.58, P-value < 0.004). When HbA1c-related molecular networks were investigated using natural language programming algorithms, multiple genetic/small molecular (SM) pathways were highlighted as connectors between the HbA1c levels and the development of NAFLD, including ones for nitric oxide, hypoxia and receptor for advanced glycation end products (RAGE). Our results suggest that increased levels of HbA1c may contribute to the progression of NAFLD either directly, by stimulating RAGE or indirectly, through the promotion of hypoxia and suppression of the release of NO. Further studies are needed to test the impact of HbA1c on the development of the chronic liver disease.
format Online
Article
Text
id pubmed-6997109
institution National Center for Biotechnology Information
language English
publishDate 2020
publisher Portland Press Ltd.
record_format MEDLINE/PubMed
spelling pubmed-69971092020-02-10 HbA1c may contribute to the development of non-alcoholic fatty liver disease even at normal-range levels Chen, Changxi Zhu, Zhongwei Mao, Yushan Xu, Yimin Du, Juan Tang, Xiaoping Cao, Hongbao Biosci Rep Bioinformatics Previous clinical studies highlighted nonalcoholic fatty liver disease (NAFLD) as a hepatic facet of metabolic syndrome, which progresses toward Type 2 diabetes along with an elevation of HbA1c in the blood. Longitudinal observations were performed in a cohort of 2811 participants with no liver disease at inception. The rate of the conversion into NAFLD was 15.7% (440/2811), with a steady increase in prevalence observed in sub-cohorts with increasing HbA1c levels. Moreover, regression analysis indicated that HbA1c levels serve as the risk factors for NAFLD after multiple adjustments (odds ratio: 1.58, P-value < 0.004). When HbA1c-related molecular networks were investigated using natural language programming algorithms, multiple genetic/small molecular (SM) pathways were highlighted as connectors between the HbA1c levels and the development of NAFLD, including ones for nitric oxide, hypoxia and receptor for advanced glycation end products (RAGE). Our results suggest that increased levels of HbA1c may contribute to the progression of NAFLD either directly, by stimulating RAGE or indirectly, through the promotion of hypoxia and suppression of the release of NO. Further studies are needed to test the impact of HbA1c on the development of the chronic liver disease. Portland Press Ltd. 2020-01-31 /pmc/articles/PMC6997109/ /pubmed/31940026 http://dx.doi.org/10.1042/BSR20193996 Text en © 2020 The Author(s). https://creativecommons.org/licenses/by/4.0/ This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY).
spellingShingle Bioinformatics
Chen, Changxi
Zhu, Zhongwei
Mao, Yushan
Xu, Yimin
Du, Juan
Tang, Xiaoping
Cao, Hongbao
HbA1c may contribute to the development of non-alcoholic fatty liver disease even at normal-range levels
title HbA1c may contribute to the development of non-alcoholic fatty liver disease even at normal-range levels
title_full HbA1c may contribute to the development of non-alcoholic fatty liver disease even at normal-range levels
title_fullStr HbA1c may contribute to the development of non-alcoholic fatty liver disease even at normal-range levels
title_full_unstemmed HbA1c may contribute to the development of non-alcoholic fatty liver disease even at normal-range levels
title_short HbA1c may contribute to the development of non-alcoholic fatty liver disease even at normal-range levels
title_sort hba1c may contribute to the development of non-alcoholic fatty liver disease even at normal-range levels
topic Bioinformatics
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6997109/
https://www.ncbi.nlm.nih.gov/pubmed/31940026
http://dx.doi.org/10.1042/BSR20193996
work_keys_str_mv AT chenchangxi hba1cmaycontributetothedevelopmentofnonalcoholicfattyliverdiseaseevenatnormalrangelevels
AT zhuzhongwei hba1cmaycontributetothedevelopmentofnonalcoholicfattyliverdiseaseevenatnormalrangelevels
AT maoyushan hba1cmaycontributetothedevelopmentofnonalcoholicfattyliverdiseaseevenatnormalrangelevels
AT xuyimin hba1cmaycontributetothedevelopmentofnonalcoholicfattyliverdiseaseevenatnormalrangelevels
AT dujuan hba1cmaycontributetothedevelopmentofnonalcoholicfattyliverdiseaseevenatnormalrangelevels
AT tangxiaoping hba1cmaycontributetothedevelopmentofnonalcoholicfattyliverdiseaseevenatnormalrangelevels
AT caohongbao hba1cmaycontributetothedevelopmentofnonalcoholicfattyliverdiseaseevenatnormalrangelevels