High Fat Diet Alters Gut Microbiota and the Expression of Paneth Cell-Antimicrobial Peptides Preceding Changes of Circulating Inflammatory Cytokines

Obesity is an established risk factor for many diseases including intestinal cancer. One of the responsible mechanisms is the chronic inflammation driven by obesity. However, it remains to be defined whether diet-induced obesity exacerbates the intestinal inflammatory status by cytokines produced in...

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Main Authors: Xiulan Guo, Jinchao Li, Renyong Tang, Guodong Zhang, Huawei Zeng, Richard J. Wood, Zhenhua Liu
Format: Article
Language:English
Published: Hindawi Limited 2017-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2017/9474896
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spelling doaj-d78862483dc94eeea57319793bc428e02020-11-25T00:28:30ZengHindawi LimitedMediators of Inflammation0962-93511466-18612017-01-01201710.1155/2017/94748969474896High Fat Diet Alters Gut Microbiota and the Expression of Paneth Cell-Antimicrobial Peptides Preceding Changes of Circulating Inflammatory CytokinesXiulan Guo0Jinchao Li1Renyong Tang2Guodong Zhang3Huawei Zeng4Richard J. Wood5Zhenhua Liu6School of Pharmacy and Biological Engineering, Chengdu University, Sichuan, ChinaSchool of Public Health and Health Sciences, University of Massachusetts, Amherst, MA, USASchool of Pharmacy and Biological Engineering, Chengdu University, Sichuan, ChinaDepartment of Food Science, University of Massachusetts, Amherst, MA, USAGrand Forks Human Nutrition Research Center, Agricultural Research Service, United States Department of Agriculture, Grand Forks, ND, USASchool of Public Health and Health Sciences, University of Massachusetts, Amherst, MA, USASchool of Public Health and Health Sciences, University of Massachusetts, Amherst, MA, USAObesity is an established risk factor for many diseases including intestinal cancer. One of the responsible mechanisms is the chronic inflammation driven by obesity. However, it remains to be defined whether diet-induced obesity exacerbates the intestinal inflammatory status by cytokines produced in adipose tissue or the high fat diet first alters the gut microbiota and then drives intestinal inflammation. To address this question, we fed C57BL/6 mice with a high fat diet (HF, 60%) and sacrificed them sequentially after 8, 12, and 16 weeks, and then compositions of gut microbiota and expressions of antimicrobial peptides were determined. The compositions of gut microbiota were altered at 8 wk HF feeding, followed with reduced Paneth antimicrobial peptides lysozyme and Reg IIIγ after 12 and 16 wk HF feeding (p<0.05), whereas elevations of circulating inflammatory cytokines IFNγ and TNF-α were observed until feeding a HF diet for 16 weeks (p<0.05). These results indicated that high fat diet may stimulate intestinal inflammation via altering gut microbiota, and it occurs prior to the potential influence by circulating inflammatory cytokines. These findings emphasized the importance of microbiota, in addition to adipose tissue per se, in driving intestinal inflammation, which may thereafter promote intestinal tumorigenesis.http://dx.doi.org/10.1155/2017/9474896
collection DOAJ
language English
format Article
sources DOAJ
author Xiulan Guo
Jinchao Li
Renyong Tang
Guodong Zhang
Huawei Zeng
Richard J. Wood
Zhenhua Liu
spellingShingle Xiulan Guo
Jinchao Li
Renyong Tang
Guodong Zhang
Huawei Zeng
Richard J. Wood
Zhenhua Liu
High Fat Diet Alters Gut Microbiota and the Expression of Paneth Cell-Antimicrobial Peptides Preceding Changes of Circulating Inflammatory Cytokines
Mediators of Inflammation
author_facet Xiulan Guo
Jinchao Li
Renyong Tang
Guodong Zhang
Huawei Zeng
Richard J. Wood
Zhenhua Liu
author_sort Xiulan Guo
title High Fat Diet Alters Gut Microbiota and the Expression of Paneth Cell-Antimicrobial Peptides Preceding Changes of Circulating Inflammatory Cytokines
title_short High Fat Diet Alters Gut Microbiota and the Expression of Paneth Cell-Antimicrobial Peptides Preceding Changes of Circulating Inflammatory Cytokines
title_full High Fat Diet Alters Gut Microbiota and the Expression of Paneth Cell-Antimicrobial Peptides Preceding Changes of Circulating Inflammatory Cytokines
title_fullStr High Fat Diet Alters Gut Microbiota and the Expression of Paneth Cell-Antimicrobial Peptides Preceding Changes of Circulating Inflammatory Cytokines
title_full_unstemmed High Fat Diet Alters Gut Microbiota and the Expression of Paneth Cell-Antimicrobial Peptides Preceding Changes of Circulating Inflammatory Cytokines
title_sort high fat diet alters gut microbiota and the expression of paneth cell-antimicrobial peptides preceding changes of circulating inflammatory cytokines
publisher Hindawi Limited
series Mediators of Inflammation
issn 0962-9351
1466-1861
publishDate 2017-01-01
description Obesity is an established risk factor for many diseases including intestinal cancer. One of the responsible mechanisms is the chronic inflammation driven by obesity. However, it remains to be defined whether diet-induced obesity exacerbates the intestinal inflammatory status by cytokines produced in adipose tissue or the high fat diet first alters the gut microbiota and then drives intestinal inflammation. To address this question, we fed C57BL/6 mice with a high fat diet (HF, 60%) and sacrificed them sequentially after 8, 12, and 16 weeks, and then compositions of gut microbiota and expressions of antimicrobial peptides were determined. The compositions of gut microbiota were altered at 8 wk HF feeding, followed with reduced Paneth antimicrobial peptides lysozyme and Reg IIIγ after 12 and 16 wk HF feeding (p<0.05), whereas elevations of circulating inflammatory cytokines IFNγ and TNF-α were observed until feeding a HF diet for 16 weeks (p<0.05). These results indicated that high fat diet may stimulate intestinal inflammation via altering gut microbiota, and it occurs prior to the potential influence by circulating inflammatory cytokines. These findings emphasized the importance of microbiota, in addition to adipose tissue per se, in driving intestinal inflammation, which may thereafter promote intestinal tumorigenesis.
url http://dx.doi.org/10.1155/2017/9474896
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