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Gut Microbiota and Type 2 Diabetes Mellitus: Association, Mechanism, and Translational Applications
Gut microbiota has attracted widespread attention due to its crucial role in disease pathophysiology, including type 2 diabetes mellitus (T2DM). Metabolites and bacterial components of gut microbiota affect the initiation and progression of T2DM by regulating inflammation, immunity, and metabolism....
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Published in: | Mediators of inflammation 2021-08, Vol.2021, p.5110276-12 |
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description | Gut microbiota has attracted widespread attention due to its crucial role in disease pathophysiology, including type 2 diabetes mellitus (T2DM). Metabolites and bacterial components of gut microbiota affect the initiation and progression of T2DM by regulating inflammation, immunity, and metabolism. Short-chain fatty acids, secondary bile acid, imidazole propionate, branched-chain amino acids, and lipopolysaccharide are the main molecules related to T2DM. Many studies have investigated the role of gut microbiota in T2DM, particularly those butyrate-producing bacteria. Increasing evidence has demonstrated that fecal microbiota transplantation and probiotic capsules are useful strategies in preventing diabetes. In this review, we aim to elucidate the complex association between gut microbiota and T2DM inflammation, metabolism, and immune disorders, the underlying mechanisms, and translational applications of gut microbiota. This review will provide novel insight into developing individualized therapy for T2DM patients based on gut microbiota immunometabolism. |
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Metabolites and bacterial components of gut microbiota affect the initiation and progression of T2DM by regulating inflammation, immunity, and metabolism. Short-chain fatty acids, secondary bile acid, imidazole propionate, branched-chain amino acids, and lipopolysaccharide are the main molecules related to T2DM. Many studies have investigated the role of gut microbiota in T2DM, particularly those butyrate-producing bacteria. Increasing evidence has demonstrated that fecal microbiota transplantation and probiotic capsules are useful strategies in preventing diabetes. In this review, we aim to elucidate the complex association between gut microbiota and T2DM inflammation, metabolism, and immune disorders, the underlying mechanisms, and translational applications of gut microbiota. This review will provide novel insight into developing individualized therapy for T2DM patients based on gut microbiota immunometabolism.</description><identifier>ISSN: 0962-9351</identifier><identifier>EISSN: 1466-1861</identifier><identifier>DOI: 10.1155/2021/5110276</identifier><identifier>PMID: 34447287</identifier><language>eng</language><publisher>United States: Hindawi</publisher><subject>Bacteria ; Branched chain amino acids ; Deoxycholic acid ; Diabetes ; Diabetes mellitus (non-insulin dependent) ; Diabetes Mellitus, Type 2 - metabolism ; Disease ; Esters ; Fatty acids ; Fatty Acids, Volatile ; Fecal Microbiota Transplantation ; Fecal microflora ; Gastrointestinal Microbiome - physiology ; Glucose ; Humans ; Imidazole ; Inflammation ; Insulin resistance ; Intestinal microflora ; Lipopolysaccharides ; Metabolic disorders ; Metabolites ; Microbiota ; Microbiota (Symbiotic organisms) ; Pathogenesis ; Physiological aspects ; Prevention ; Probiotics ; Probiotics - therapeutic use ; Propionic acid ; Review ; Translation ; Transplantation ; Type 2 diabetes</subject><ispartof>Mediators of inflammation, 2021-08, Vol.2021, p.5110276-12</ispartof><rights>Copyright © 2021 Lili Zhang et al.</rights><rights>COPYRIGHT 2021 John Wiley & Sons, Inc.</rights><rights>Copyright © 2021 Lili Zhang et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2021 Lili Zhang et al. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c581t-e52df67af2383b5ec4e14eb3601a5ff292cdeb4ca0c6c87da0d7d4199b1979c83</citedby><cites>FETCH-LOGICAL-c581t-e52df67af2383b5ec4e14eb3601a5ff292cdeb4ca0c6c87da0d7d4199b1979c83</cites><orcidid>0000-0003-3264-0881 ; 0000-0002-1170-6805</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2565925162/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2565925162?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34447287$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Gu, Bingjie</contributor><contributor>Bingjie Gu</contributor><creatorcontrib>Zhang, Lili</creatorcontrib><creatorcontrib>Chu, Jinjin</creatorcontrib><creatorcontrib>Hao, Wenhao</creatorcontrib><creatorcontrib>Zhang, Jiaojiao</creatorcontrib><creatorcontrib>Li, Haibo</creatorcontrib><creatorcontrib>Yang, Chunjuan</creatorcontrib><creatorcontrib>Yang, Jinghan</creatorcontrib><creatorcontrib>Chen, Xiaohua</creatorcontrib><creatorcontrib>Wang, Honggang</creatorcontrib><title>Gut Microbiota and Type 2 Diabetes Mellitus: Association, Mechanism, and Translational Applications</title><title>Mediators of inflammation</title><addtitle>Mediators Inflamm</addtitle><description>Gut microbiota has attracted widespread attention due to its crucial role in disease pathophysiology, including type 2 diabetes mellitus (T2DM). Metabolites and bacterial components of gut microbiota affect the initiation and progression of T2DM by regulating inflammation, immunity, and metabolism. Short-chain fatty acids, secondary bile acid, imidazole propionate, branched-chain amino acids, and lipopolysaccharide are the main molecules related to T2DM. Many studies have investigated the role of gut microbiota in T2DM, particularly those butyrate-producing bacteria. Increasing evidence has demonstrated that fecal microbiota transplantation and probiotic capsules are useful strategies in preventing diabetes. In this review, we aim to elucidate the complex association between gut microbiota and T2DM inflammation, metabolism, and immune disorders, the underlying mechanisms, and translational applications of gut microbiota. This review will provide novel insight into developing individualized therapy for T2DM patients based on gut microbiota immunometabolism.</description><subject>Bacteria</subject><subject>Branched chain amino acids</subject><subject>Deoxycholic acid</subject><subject>Diabetes</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Disease</subject><subject>Esters</subject><subject>Fatty acids</subject><subject>Fatty Acids, Volatile</subject><subject>Fecal Microbiota Transplantation</subject><subject>Fecal microflora</subject><subject>Gastrointestinal Microbiome - physiology</subject><subject>Glucose</subject><subject>Humans</subject><subject>Imidazole</subject><subject>Inflammation</subject><subject>Insulin resistance</subject><subject>Intestinal microflora</subject><subject>Lipopolysaccharides</subject><subject>Metabolic disorders</subject><subject>Metabolites</subject><subject>Microbiota</subject><subject>Microbiota (Symbiotic organisms)</subject><subject>Pathogenesis</subject><subject>Physiological aspects</subject><subject>Prevention</subject><subject>Probiotics</subject><subject>Probiotics - therapeutic use</subject><subject>Propionic acid</subject><subject>Review</subject><subject>Translation</subject><subject>Transplantation</subject><subject>Type 2 diabetes</subject><issn>0962-9351</issn><issn>1466-1861</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNp9ks1v1DAQxSMEotvCjTOKxAWpu62_43BAWhUolVpxKWdr4ox3vUriECeg_vd4PygsQsgHyzO_ebafXpa9ouSCUikvGWH0UlJKWKGeZDMqlFpQrejTbEZKxRYll_QkO41xQwiRQujn2QkXQhRMF7PMXk9jfuftECofRsihq_P7hx5zln_wUOGIMb_DpvHjFN_lyxiD9TD60M1T2a6h87Gd76cG6GKz60GTL_u-8XZ3ii-yZw6aiC8P-1n29dPH-6vPi9sv1zdXy9uFlZqOC5SsdqoAx7jmlUQrkAqsuCIUpHOsZLbGSlggVlld1EDqoha0LCtaFqXV_Cy72evWATamH3wLw4MJ4M2uEIaVgWH0tkFDILklZMkdQcE0BYYVIQ4Ly3nhHE9a7_da_VS1WFvsxgGaI9HjTufXZhW-G821kEwkgbcHgSF8mzCOpvXRJiehwzBFw6RShAvNtu9-8xe6CdOQXNxRsmSSKvabWkH6gO9cSPfarahZqlLpgikpE3XxDyqtGltvQ4fOp_rRwHw_kCIQ44Du8Y-UmG3AzDZg5hCwhL_-05dH-FeiEnC-B9a-q-GH_7_cT_hd1m4</recordid><startdate>20210817</startdate><enddate>20210817</enddate><creator>Zhang, Lili</creator><creator>Chu, Jinjin</creator><creator>Hao, Wenhao</creator><creator>Zhang, Jiaojiao</creator><creator>Li, Haibo</creator><creator>Yang, Chunjuan</creator><creator>Yang, Jinghan</creator><creator>Chen, Xiaohua</creator><creator>Wang, Honggang</creator><general>Hindawi</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0003-3264-0881</orcidid><orcidid>https://orcid.org/0000-0002-1170-6805</orcidid></search><sort><creationdate>20210817</creationdate><title>Gut Microbiota and Type 2 Diabetes Mellitus: Association, Mechanism, and Translational Applications</title><author>Zhang, Lili ; Chu, Jinjin ; Hao, Wenhao ; Zhang, Jiaojiao ; Li, Haibo ; Yang, Chunjuan ; Yang, Jinghan ; Chen, Xiaohua ; Wang, Honggang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c581t-e52df67af2383b5ec4e14eb3601a5ff292cdeb4ca0c6c87da0d7d4199b1979c83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Bacteria</topic><topic>Branched chain amino acids</topic><topic>Deoxycholic acid</topic><topic>Diabetes</topic><topic>Diabetes mellitus (non-insulin dependent)</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>Disease</topic><topic>Esters</topic><topic>Fatty acids</topic><topic>Fatty Acids, Volatile</topic><topic>Fecal Microbiota Transplantation</topic><topic>Fecal microflora</topic><topic>Gastrointestinal Microbiome - physiology</topic><topic>Glucose</topic><topic>Humans</topic><topic>Imidazole</topic><topic>Inflammation</topic><topic>Insulin resistance</topic><topic>Intestinal microflora</topic><topic>Lipopolysaccharides</topic><topic>Metabolic disorders</topic><topic>Metabolites</topic><topic>Microbiota</topic><topic>Microbiota (Symbiotic organisms)</topic><topic>Pathogenesis</topic><topic>Physiological aspects</topic><topic>Prevention</topic><topic>Probiotics</topic><topic>Probiotics - therapeutic use</topic><topic>Propionic acid</topic><topic>Review</topic><topic>Translation</topic><topic>Transplantation</topic><topic>Type 2 diabetes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Lili</creatorcontrib><creatorcontrib>Chu, Jinjin</creatorcontrib><creatorcontrib>Hao, Wenhao</creatorcontrib><creatorcontrib>Zhang, Jiaojiao</creatorcontrib><creatorcontrib>Li, Haibo</creatorcontrib><creatorcontrib>Yang, Chunjuan</creatorcontrib><creatorcontrib>Yang, Jinghan</creatorcontrib><creatorcontrib>Chen, Xiaohua</creatorcontrib><creatorcontrib>Wang, Honggang</creatorcontrib><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest Health and Medical</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest research library</collection><collection>ProQuest Biological Science Journals</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Mediators of inflammation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Lili</au><au>Chu, Jinjin</au><au>Hao, Wenhao</au><au>Zhang, Jiaojiao</au><au>Li, Haibo</au><au>Yang, Chunjuan</au><au>Yang, Jinghan</au><au>Chen, Xiaohua</au><au>Wang, Honggang</au><au>Gu, Bingjie</au><au>Bingjie Gu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Gut Microbiota and Type 2 Diabetes Mellitus: Association, Mechanism, and Translational Applications</atitle><jtitle>Mediators of inflammation</jtitle><addtitle>Mediators Inflamm</addtitle><date>2021-08-17</date><risdate>2021</risdate><volume>2021</volume><spage>5110276</spage><epage>12</epage><pages>5110276-12</pages><issn>0962-9351</issn><eissn>1466-1861</eissn><abstract>Gut microbiota has attracted widespread attention due to its crucial role in disease pathophysiology, including type 2 diabetes mellitus (T2DM). Metabolites and bacterial components of gut microbiota affect the initiation and progression of T2DM by regulating inflammation, immunity, and metabolism. Short-chain fatty acids, secondary bile acid, imidazole propionate, branched-chain amino acids, and lipopolysaccharide are the main molecules related to T2DM. Many studies have investigated the role of gut microbiota in T2DM, particularly those butyrate-producing bacteria. Increasing evidence has demonstrated that fecal microbiota transplantation and probiotic capsules are useful strategies in preventing diabetes. In this review, we aim to elucidate the complex association between gut microbiota and T2DM inflammation, metabolism, and immune disorders, the underlying mechanisms, and translational applications of gut microbiota. This review will provide novel insight into developing individualized therapy for T2DM patients based on gut microbiota immunometabolism.</abstract><cop>United States</cop><pub>Hindawi</pub><pmid>34447287</pmid><doi>10.1155/2021/5110276</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0003-3264-0881</orcidid><orcidid>https://orcid.org/0000-0002-1170-6805</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Bacteria Branched chain amino acids Deoxycholic acid Diabetes Diabetes mellitus (non-insulin dependent) Diabetes Mellitus, Type 2 - metabolism Disease Esters Fatty acids Fatty Acids, Volatile Fecal Microbiota Transplantation Fecal microflora Gastrointestinal Microbiome - physiology Glucose Humans Imidazole Inflammation Insulin resistance Intestinal microflora Lipopolysaccharides Metabolic disorders Metabolites Microbiota Microbiota (Symbiotic organisms) Pathogenesis Physiological aspects Prevention Probiotics Probiotics - therapeutic use Propionic acid Review Translation Transplantation Type 2 diabetes |
title | Gut Microbiota and Type 2 Diabetes Mellitus: Association, Mechanism, and Translational Applications |
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