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AMPKα pathway involved in hepatic triglyceride metabolism disorder in diet-induced obesity mice following Escherichia coli Infection

To investigate the different effects of acute pulmonary infection induced by Escherichia coli (E. coli) on lipid metabolism between diet-induced obesity (DIO, fed with high-fat diet) mice and lean mice. A total of 180 ICR mice were selected to be challenged intranasally with phosphate-buffered salin...

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Autores principales: Fang, Jing, Wang, Fengyuan, Song, Hetao, Wang, Zhengyi, Zuo, Zhicai, Cui, Hengmin, Jia, Yiping, Deng, Junliang, Yu, Shumin, Hu, Yanchun, Shen, Liuhong, Ma, Xiaoping, Ren, Zhihua, Gou, Liping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6286859/
https://www.ncbi.nlm.nih.gov/pubmed/30398974
http://dx.doi.org/10.18632/aging.101623
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author Fang, Jing
Wang, Fengyuan
Song, Hetao
Wang, Zhengyi
Zuo, Zhicai
Cui, Hengmin
Jia, Yiping
Deng, Junliang
Yu, Shumin
Hu, Yanchun
Shen, Liuhong
Ma, Xiaoping
Ren, Zhihua
Gou, Liping
author_facet Fang, Jing
Wang, Fengyuan
Song, Hetao
Wang, Zhengyi
Zuo, Zhicai
Cui, Hengmin
Jia, Yiping
Deng, Junliang
Yu, Shumin
Hu, Yanchun
Shen, Liuhong
Ma, Xiaoping
Ren, Zhihua
Gou, Liping
author_sort Fang, Jing
collection PubMed
description To investigate the different effects of acute pulmonary infection induced by Escherichia coli (E. coli) on lipid metabolism between diet-induced obesity (DIO, fed with high-fat diet) mice and lean mice. A total of 180 ICR mice were selected to be challenged intranasally with phosphate-buffered saline or 10(9) CFUs/mL of E. coli, and the body character indexes, biochemical indexes and expressions of genes and proteins involved in lipid metabolism were examined pre- and post-infection. Results revealed that, before infection, DIO mice had significantly higher body weight, adipose and liver indexes, free fatty acid and triglyceride contents than lean mice. After infection, increased free fatty acid and triglyceride contents, increased expressions of resistin, SREBP-1c, ACC1, FAS and SCD-1, and declined PPARα, CPT-1α expressions and AMPKα phosphorylation were detected in the infected group, while the change rates were more serious in the lean mice than the DIO mice. The above-mentioned findings verified that, after being infected with E. coli, hepatic lipid metabolism disorder was aggravated by activating SREBP-1c related lipid synthesis pathway and inhibiting PPARα related fatty acid oxidation pathway. However, infection-induced lipid metabolic disorders was slighter in the DIO mice than the lean mice through AMPKα pathway.
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spelling pubmed-62868592018-12-17 AMPKα pathway involved in hepatic triglyceride metabolism disorder in diet-induced obesity mice following Escherichia coli Infection Fang, Jing Wang, Fengyuan Song, Hetao Wang, Zhengyi Zuo, Zhicai Cui, Hengmin Jia, Yiping Deng, Junliang Yu, Shumin Hu, Yanchun Shen, Liuhong Ma, Xiaoping Ren, Zhihua Gou, Liping Aging (Albany NY) Research Paper To investigate the different effects of acute pulmonary infection induced by Escherichia coli (E. coli) on lipid metabolism between diet-induced obesity (DIO, fed with high-fat diet) mice and lean mice. A total of 180 ICR mice were selected to be challenged intranasally with phosphate-buffered saline or 10(9) CFUs/mL of E. coli, and the body character indexes, biochemical indexes and expressions of genes and proteins involved in lipid metabolism were examined pre- and post-infection. Results revealed that, before infection, DIO mice had significantly higher body weight, adipose and liver indexes, free fatty acid and triglyceride contents than lean mice. After infection, increased free fatty acid and triglyceride contents, increased expressions of resistin, SREBP-1c, ACC1, FAS and SCD-1, and declined PPARα, CPT-1α expressions and AMPKα phosphorylation were detected in the infected group, while the change rates were more serious in the lean mice than the DIO mice. The above-mentioned findings verified that, after being infected with E. coli, hepatic lipid metabolism disorder was aggravated by activating SREBP-1c related lipid synthesis pathway and inhibiting PPARα related fatty acid oxidation pathway. However, infection-induced lipid metabolic disorders was slighter in the DIO mice than the lean mice through AMPKα pathway. Impact Journals 2018-11-06 /pmc/articles/PMC6286859/ /pubmed/30398974 http://dx.doi.org/10.18632/aging.101623 Text en Copyright © 2018 Fang et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution (CC BY) 3.0 License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Paper
Fang, Jing
Wang, Fengyuan
Song, Hetao
Wang, Zhengyi
Zuo, Zhicai
Cui, Hengmin
Jia, Yiping
Deng, Junliang
Yu, Shumin
Hu, Yanchun
Shen, Liuhong
Ma, Xiaoping
Ren, Zhihua
Gou, Liping
AMPKα pathway involved in hepatic triglyceride metabolism disorder in diet-induced obesity mice following Escherichia coli Infection
title AMPKα pathway involved in hepatic triglyceride metabolism disorder in diet-induced obesity mice following Escherichia coli Infection
title_full AMPKα pathway involved in hepatic triglyceride metabolism disorder in diet-induced obesity mice following Escherichia coli Infection
title_fullStr AMPKα pathway involved in hepatic triglyceride metabolism disorder in diet-induced obesity mice following Escherichia coli Infection
title_full_unstemmed AMPKα pathway involved in hepatic triglyceride metabolism disorder in diet-induced obesity mice following Escherichia coli Infection
title_short AMPKα pathway involved in hepatic triglyceride metabolism disorder in diet-induced obesity mice following Escherichia coli Infection
title_sort ampkα pathway involved in hepatic triglyceride metabolism disorder in diet-induced obesity mice following escherichia coli infection
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6286859/
https://www.ncbi.nlm.nih.gov/pubmed/30398974
http://dx.doi.org/10.18632/aging.101623
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