Intermittent Fasting Improves Insulin Resistance by Modulating the Gut Microbiota and Bile Acid Metabolism in Diet-Induced Obesity

IF 4.5 2区 农林科学 Q1 FOOD SCIENCE & TECHNOLOGY
Sha Lei, Guanghui Liu, Shouli Wang, Guannan Zong, Xiaoya Zhang, Lingling Pan, Junfeng Han
{"title":"Intermittent Fasting Improves Insulin Resistance by Modulating the Gut Microbiota and Bile Acid Metabolism in Diet-Induced Obesity","authors":"Sha Lei,&nbsp;Guanghui Liu,&nbsp;Shouli Wang,&nbsp;Guannan Zong,&nbsp;Xiaoya Zhang,&nbsp;Lingling Pan,&nbsp;Junfeng Han","doi":"10.1002/mnfr.202400451","DOIUrl":null,"url":null,"abstract":"<div>\n \n <section>\n \n <h3> Scope</h3>\n \n <p>Adipose tissue macrophages (ATMs) are crucial in the pathogenesis of insulin resistance (IR). Intermittent fasting (IF) is an effective intervention for obesity. However, the underlying mechanism by which IF improves IR remains unclear.</p>\n </section>\n \n <section>\n \n <h3> Methods and results</h3>\n \n <p>Male C57BL/6J mice are fed chow-diet and high-fat diet (HFD) for 12 weeks, then is randomized into ad libitum feeding or every other day fasting for 8 weeks. Markers of ATMs and expression of uncoupling protein 1 (UCP-1) are determined. Gut microbiota and bile acids (BAs) are profiled using 16S rRNA sequencing and targeted metabolomics analysis. Results indicate that IF improves IR in HFD-induced obesity. IF decreases ATM infiltration, pro-inflammatory M1 gene expression, and promotes white adipose tissue (WAT) browning by elevating UCP-1 expression. IF restructures microbiota composition, significantly expanding the abundance of <i>Verrucomicrobia</i> particularly <i>Akkermansia muciniphila</i>, with the decrease of that of <i>Firmicutes</i>. IF increases the level of total BAs and alters the composition of BAs with higher proportion of 12α-hydroxylated (12α-OH) BAs. The changes in these BAs are correlated with differential bacteria.</p>\n </section>\n \n <section>\n \n <h3> Conclusion</h3>\n \n <p>The findings indicate that IF improves IR partially mediated by the interplay between restructured gut microbiota and BAs metabolism, which has implications for the dietary management in obesity.</p>\n </section>\n </div>","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"68 22","pages":""},"PeriodicalIF":4.5000,"publicationDate":"2024-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mnfr.202400451","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular Nutrition & Food Research","FirstCategoryId":"97","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/mnfr.202400451","RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"FOOD SCIENCE & TECHNOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Scope

Adipose tissue macrophages (ATMs) are crucial in the pathogenesis of insulin resistance (IR). Intermittent fasting (IF) is an effective intervention for obesity. However, the underlying mechanism by which IF improves IR remains unclear.

Methods and results

Male C57BL/6J mice are fed chow-diet and high-fat diet (HFD) for 12 weeks, then is randomized into ad libitum feeding or every other day fasting for 8 weeks. Markers of ATMs and expression of uncoupling protein 1 (UCP-1) are determined. Gut microbiota and bile acids (BAs) are profiled using 16S rRNA sequencing and targeted metabolomics analysis. Results indicate that IF improves IR in HFD-induced obesity. IF decreases ATM infiltration, pro-inflammatory M1 gene expression, and promotes white adipose tissue (WAT) browning by elevating UCP-1 expression. IF restructures microbiota composition, significantly expanding the abundance of Verrucomicrobia particularly Akkermansia muciniphila, with the decrease of that of Firmicutes. IF increases the level of total BAs and alters the composition of BAs with higher proportion of 12α-hydroxylated (12α-OH) BAs. The changes in these BAs are correlated with differential bacteria.

Conclusion

The findings indicate that IF improves IR partially mediated by the interplay between restructured gut microbiota and BAs metabolism, which has implications for the dietary management in obesity.

Abstract Image

Abstract Image

间歇性禁食通过调节饮食诱发肥胖症患者的肠道微生物群和胆汁酸代谢改善胰岛素抵抗
范围脂肪组织巨噬细胞(ATMs)在胰岛素抵抗(IR)的发病机制中至关重要。间歇性禁食(IF)是一种有效的肥胖干预措施。方法和结果将雄性C57BL/6J小鼠饲喂饲料和高脂饮食(HFD)12周,然后随机分为自由进食或隔日禁食8周。测定 ATMs 标记和解偶联蛋白 1(UCP-1)的表达。利用 16S rRNA 测序和靶向代谢组学分析对肠道微生物群和胆汁酸(BAs)进行分析。结果表明,IF 能改善高氟酸膳食诱导的肥胖症的 IR。IF 可减少 ATM 的浸润、促炎 M1 基因的表达,并通过提高 UCP-1 的表达促进白色脂肪组织(WAT)褐变。IF 重构了微生物群的组成,显著增加了纤毛虫(Verrucomicrobia),尤其是 Akkermansia muciniphila 的数量,同时减少了固着菌(Firmicutes)的数量。IF 增加了 BAs 的总量,并改变了 BAs 的组成,12α-羟基化(12α-OH)BAs 的比例更高。研究结果表明,肠道微生物群重组与 BAs 代谢之间的相互作用部分介导了 IF 对 IR 的改善,这对肥胖症的饮食管理具有重要意义。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Molecular Nutrition & Food Research
Molecular Nutrition & Food Research 工程技术-食品科技
CiteScore
8.70
自引率
1.90%
发文量
250
审稿时长
1.7 months
期刊介绍: Molecular Nutrition & Food Research is a primary research journal devoted to health, safety and all aspects of molecular nutrition such as nutritional biochemistry, nutrigenomics and metabolomics aiming to link the information arising from related disciplines: Bioactivity: Nutritional and medical effects of food constituents including bioavailability and kinetics. Immunology: Understanding the interactions of food and the immune system. Microbiology: Food spoilage, food pathogens, chemical and physical approaches of fermented foods and novel microbial processes. Chemistry: Isolation and analysis of bioactive food ingredients while considering environmental aspects.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信