Gut microbiota, probiotics and diabetes
Diabetes is a condition of multifactorial origin, involving several molecular mechanisms related to the intestinal microbiota for its development. In type 2 diabetes, receptor activation and recognition by microorganisms from the intestinal lumen may trigger inflammatory responses, inducing the phos...
Gespeichert in:
| Veröffentlicht in: | Nutrition journal 2014-06, Vol.13 (1), p.60-60, Article 60 |
|---|---|
| Hauptverfasser: | , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 60 |
|---|---|
| container_issue | 1 |
| container_start_page | 60 |
| container_title | Nutrition journal |
| container_volume | 13 |
| creator | Gomes, Aline Corado Bueno, Allain Amador de Souza, Rávila Graziany Machado Mota, João Felipe |
| description | Diabetes is a condition of multifactorial origin, involving several molecular mechanisms related to the intestinal microbiota for its development. In type 2 diabetes, receptor activation and recognition by microorganisms from the intestinal lumen may trigger inflammatory responses, inducing the phosphorylation of serine residues in insulin receptor substrate-1, reducing insulin sensitivity. In type 1 diabetes, the lowered expression of adhesion proteins within the intestinal epithelium favours a greater immune response that may result in destruction of pancreatic β cells by CD8+ T-lymphocytes, and increased expression of interleukin-17, related to autoimmunity. Research in animal models and humans has hypothesized whether the administration of probiotics may improve the prognosis of diabetes through modulation of gut microbiota. We have shown in this review that a large body of evidence suggests probiotics reduce the inflammatory response and oxidative stress, as well as increase the expression of adhesion proteins within the intestinal epithelium, reducing intestinal permeability. Such effects increase insulin sensitivity and reduce autoimmune response. However, further investigations are required to clarify whether the administration of probiotics can be efficiently used for the prevention and management of diabetes. |
| doi_str_mv | 10.1186/1475-2891-13-60 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4078018</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A539675915</galeid><sourcerecordid>A539675915</sourcerecordid><originalsourceid>FETCH-LOGICAL-b671t-c5fa4a97264b06d843863617f39d854e93df090fe55c99440f465048cd282c443</originalsourceid><addsrcrecordid>eNqNkt9rFDEQxxdR7A999k0PfKiC287k1yYvQi1aCwXB2ueQzSZnyt7mutkV_e_NufW4lYqSh4SZz3zJfGeK4hnCMaIUJ8gqXhKpsERaCnhQ7G8jD3fee8VBSjcAREpVPS72CFNUgaD7xdH5OCxWwfaxDnEwbxbr6RVsWpiuWTTB1G5w6UnxyJs2uad392Fx_eH9l7OP5eWn84uz08uyFhUOpeXeMKMqIlgNopGMSkEFVp6qRnLmFG08KPCOc6sUY-CZ4MCkbYgkljF6WLyddNdjvXKNdd3Qm1av-7Ay_Q8dTdDzTBe-6mX8phlUElBmgXeTQO7iLwLzjI0rvTFKb4zSSLWALPLq7hd9vB1dGvQqJOva1nQujkmjEJRLAZL-G-UcBTJJ5H-gjGQ3JMWMvvwDvYlj32Xnf1HZXqx2qKVpnQ6dj7kjuxHVp5wqUXGFPFPH91D5NC4PPnbOhxyfFbyeFWRmcN-HpRlT0hdXn-fsycTmDUqpd37rNILerOg93j7fnfCW_72TGXgxAd5EbZZ9SPr6igAyABRQcUJ_AnFX5N0</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1542264171</pqid></control><display><type>article</type><title>Gut microbiota, probiotics and diabetes</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central Open Access</source><source>Springer Nature OA Free Journals</source><source>Springer Nature - Complete Springer Journals</source><source>PubMed Central</source><source>Free Full-Text Journals in Chemistry</source><creator>Gomes, Aline Corado ; Bueno, Allain Amador ; de Souza, Rávila Graziany Machado ; Mota, João Felipe</creator><creatorcontrib>Gomes, Aline Corado ; Bueno, Allain Amador ; de Souza, Rávila Graziany Machado ; Mota, João Felipe</creatorcontrib><description>Diabetes is a condition of multifactorial origin, involving several molecular mechanisms related to the intestinal microbiota for its development. In type 2 diabetes, receptor activation and recognition by microorganisms from the intestinal lumen may trigger inflammatory responses, inducing the phosphorylation of serine residues in insulin receptor substrate-1, reducing insulin sensitivity. In type 1 diabetes, the lowered expression of adhesion proteins within the intestinal epithelium favours a greater immune response that may result in destruction of pancreatic β cells by CD8+ T-lymphocytes, and increased expression of interleukin-17, related to autoimmunity. Research in animal models and humans has hypothesized whether the administration of probiotics may improve the prognosis of diabetes through modulation of gut microbiota. We have shown in this review that a large body of evidence suggests probiotics reduce the inflammatory response and oxidative stress, as well as increase the expression of adhesion proteins within the intestinal epithelium, reducing intestinal permeability. Such effects increase insulin sensitivity and reduce autoimmune response. However, further investigations are required to clarify whether the administration of probiotics can be efficiently used for the prevention and management of diabetes.</description><identifier>ISSN: 1475-2891</identifier><identifier>EISSN: 1475-2891</identifier><identifier>DOI: 10.1186/1475-2891-13-60</identifier><identifier>PMID: 24939063</identifier><language>eng</language><publisher>England: Springer-Verlag</publisher><subject>adhesion ; Analysis ; animal models ; Animals ; autoimmunity ; Care and treatment ; CD8-positive T-lymphocytes ; Clinical Trials as Topic ; Development and progression ; Diabetes Mellitus, Type 1 - etiology ; Diabetes Mellitus, Type 1 - therapy ; Diabetes Mellitus, Type 2 - etiology ; Diabetes Mellitus, Type 2 - therapy ; Fatty acids ; Gastrointestinal Tract - microbiology ; Humans ; Immune response ; Inflammation ; Inflammation - etiology ; Insulin ; insulin receptors ; Insulin Resistance ; insulin-dependent diabetes mellitus ; Interleukins ; intestinal microorganisms ; intestinal mucosa ; Kinases ; laboratory animals ; Lymphocytes ; Metabolic disorders ; Microbiota ; noninsulin-dependent diabetes mellitus ; Nutrition ; oxidative stress ; Pancreatic beta cells ; Patient outcomes ; permeability ; phosphorylation ; Probiotics ; Probiotics - therapeutic use ; prognosis ; Review ; serine ; Studies ; Toll-Like Receptor 4 - physiology ; Type 2 diabetes</subject><ispartof>Nutrition journal, 2014-06, Vol.13 (1), p.60-60, Article 60</ispartof><rights>COPYRIGHT 2014 BioMed Central Ltd.</rights><rights>2014 Gomes et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.</rights><rights>Copyright © 2014 Gomes et al.; licensee BioMed Central Ltd. 2014 Gomes et al.; licensee BioMed Central Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b671t-c5fa4a97264b06d843863617f39d854e93df090fe55c99440f465048cd282c443</citedby><cites>FETCH-LOGICAL-b671t-c5fa4a97264b06d843863617f39d854e93df090fe55c99440f465048cd282c443</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4078018/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4078018/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,862,883,27911,27912,53778,53780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24939063$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gomes, Aline Corado</creatorcontrib><creatorcontrib>Bueno, Allain Amador</creatorcontrib><creatorcontrib>de Souza, Rávila Graziany Machado</creatorcontrib><creatorcontrib>Mota, João Felipe</creatorcontrib><title>Gut microbiota, probiotics and diabetes</title><title>Nutrition journal</title><addtitle>Nutr J</addtitle><description>Diabetes is a condition of multifactorial origin, involving several molecular mechanisms related to the intestinal microbiota for its development. In type 2 diabetes, receptor activation and recognition by microorganisms from the intestinal lumen may trigger inflammatory responses, inducing the phosphorylation of serine residues in insulin receptor substrate-1, reducing insulin sensitivity. In type 1 diabetes, the lowered expression of adhesion proteins within the intestinal epithelium favours a greater immune response that may result in destruction of pancreatic β cells by CD8+ T-lymphocytes, and increased expression of interleukin-17, related to autoimmunity. Research in animal models and humans has hypothesized whether the administration of probiotics may improve the prognosis of diabetes through modulation of gut microbiota. We have shown in this review that a large body of evidence suggests probiotics reduce the inflammatory response and oxidative stress, as well as increase the expression of adhesion proteins within the intestinal epithelium, reducing intestinal permeability. Such effects increase insulin sensitivity and reduce autoimmune response. However, further investigations are required to clarify whether the administration of probiotics can be efficiently used for the prevention and management of diabetes.</description><subject>adhesion</subject><subject>Analysis</subject><subject>animal models</subject><subject>Animals</subject><subject>autoimmunity</subject><subject>Care and treatment</subject><subject>CD8-positive T-lymphocytes</subject><subject>Clinical Trials as Topic</subject><subject>Development and progression</subject><subject>Diabetes Mellitus, Type 1 - etiology</subject><subject>Diabetes Mellitus, Type 1 - therapy</subject><subject>Diabetes Mellitus, Type 2 - etiology</subject><subject>Diabetes Mellitus, Type 2 - therapy</subject><subject>Fatty acids</subject><subject>Gastrointestinal Tract - microbiology</subject><subject>Humans</subject><subject>Immune response</subject><subject>Inflammation</subject><subject>Inflammation - etiology</subject><subject>Insulin</subject><subject>insulin receptors</subject><subject>Insulin Resistance</subject><subject>insulin-dependent diabetes mellitus</subject><subject>Interleukins</subject><subject>intestinal microorganisms</subject><subject>intestinal mucosa</subject><subject>Kinases</subject><subject>laboratory animals</subject><subject>Lymphocytes</subject><subject>Metabolic disorders</subject><subject>Microbiota</subject><subject>noninsulin-dependent diabetes mellitus</subject><subject>Nutrition</subject><subject>oxidative stress</subject><subject>Pancreatic beta cells</subject><subject>Patient outcomes</subject><subject>permeability</subject><subject>phosphorylation</subject><subject>Probiotics</subject><subject>Probiotics - therapeutic use</subject><subject>prognosis</subject><subject>Review</subject><subject>serine</subject><subject>Studies</subject><subject>Toll-Like Receptor 4 - physiology</subject><subject>Type 2 diabetes</subject><issn>1475-2891</issn><issn>1475-2891</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNkt9rFDEQxxdR7A999k0PfKiC287k1yYvQi1aCwXB2ueQzSZnyt7mutkV_e_NufW4lYqSh4SZz3zJfGeK4hnCMaIUJ8gqXhKpsERaCnhQ7G8jD3fee8VBSjcAREpVPS72CFNUgaD7xdH5OCxWwfaxDnEwbxbr6RVsWpiuWTTB1G5w6UnxyJs2uad392Fx_eH9l7OP5eWn84uz08uyFhUOpeXeMKMqIlgNopGMSkEFVp6qRnLmFG08KPCOc6sUY-CZ4MCkbYgkljF6WLyddNdjvXKNdd3Qm1av-7Ay_Q8dTdDzTBe-6mX8phlUElBmgXeTQO7iLwLzjI0rvTFKb4zSSLWALPLq7hd9vB1dGvQqJOva1nQujkmjEJRLAZL-G-UcBTJJ5H-gjGQ3JMWMvvwDvYlj32Xnf1HZXqx2qKVpnQ6dj7kjuxHVp5wqUXGFPFPH91D5NC4PPnbOhxyfFbyeFWRmcN-HpRlT0hdXn-fsycTmDUqpd37rNILerOg93j7fnfCW_72TGXgxAd5EbZZ9SPr6igAyABRQcUJ_AnFX5N0</recordid><startdate>20140617</startdate><enddate>20140617</enddate><creator>Gomes, Aline Corado</creator><creator>Bueno, Allain Amador</creator><creator>de Souza, Rávila Graziany Machado</creator><creator>Mota, João Felipe</creator><general>Springer-Verlag</general><general>BioMed Central Ltd</general><general>BioMed Central</general><scope>FBQ</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>ISR</scope><scope>3V.</scope><scope>7QP</scope><scope>7RQ</scope><scope>7RV</scope><scope>7TS</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>7QL</scope><scope>7T7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>7S9</scope><scope>L.6</scope><scope>5PM</scope></search><sort><creationdate>20140617</creationdate><title>Gut microbiota, probiotics and diabetes</title><author>Gomes, Aline Corado ; Bueno, Allain Amador ; de Souza, Rávila Graziany Machado ; Mota, João Felipe</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b671t-c5fa4a97264b06d843863617f39d854e93df090fe55c99440f465048cd282c443</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>adhesion</topic><topic>Analysis</topic><topic>animal models</topic><topic>Animals</topic><topic>autoimmunity</topic><topic>Care and treatment</topic><topic>CD8-positive T-lymphocytes</topic><topic>Clinical Trials as Topic</topic><topic>Development and progression</topic><topic>Diabetes Mellitus, Type 1 - etiology</topic><topic>Diabetes Mellitus, Type 1 - therapy</topic><topic>Diabetes Mellitus, Type 2 - etiology</topic><topic>Diabetes Mellitus, Type 2 - therapy</topic><topic>Fatty acids</topic><topic>Gastrointestinal Tract - microbiology</topic><topic>Humans</topic><topic>Immune response</topic><topic>Inflammation</topic><topic>Inflammation - etiology</topic><topic>Insulin</topic><topic>insulin receptors</topic><topic>Insulin Resistance</topic><topic>insulin-dependent diabetes mellitus</topic><topic>Interleukins</topic><topic>intestinal microorganisms</topic><topic>intestinal mucosa</topic><topic>Kinases</topic><topic>laboratory animals</topic><topic>Lymphocytes</topic><topic>Metabolic disorders</topic><topic>Microbiota</topic><topic>noninsulin-dependent diabetes mellitus</topic><topic>Nutrition</topic><topic>oxidative stress</topic><topic>Pancreatic beta cells</topic><topic>Patient outcomes</topic><topic>permeability</topic><topic>phosphorylation</topic><topic>Probiotics</topic><topic>Probiotics - therapeutic use</topic><topic>prognosis</topic><topic>Review</topic><topic>serine</topic><topic>Studies</topic><topic>Toll-Like Receptor 4 - physiology</topic><topic>Type 2 diabetes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gomes, Aline Corado</creatorcontrib><creatorcontrib>Bueno, Allain Amador</creatorcontrib><creatorcontrib>de Souza, Rávila Graziany Machado</creatorcontrib><creatorcontrib>Mota, João Felipe</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Career & Technical Education Database</collection><collection>Nursing & Allied Health Database</collection><collection>Physical Education Index</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Public Health Database</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 Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</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>Bacteriology Abstracts (Microbiology B)</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Nutrition journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gomes, Aline Corado</au><au>Bueno, Allain Amador</au><au>de Souza, Rávila Graziany Machado</au><au>Mota, João Felipe</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Gut microbiota, probiotics and diabetes</atitle><jtitle>Nutrition journal</jtitle><addtitle>Nutr J</addtitle><date>2014-06-17</date><risdate>2014</risdate><volume>13</volume><issue>1</issue><spage>60</spage><epage>60</epage><pages>60-60</pages><artnum>60</artnum><issn>1475-2891</issn><eissn>1475-2891</eissn><abstract>Diabetes is a condition of multifactorial origin, involving several molecular mechanisms related to the intestinal microbiota for its development. In type 2 diabetes, receptor activation and recognition by microorganisms from the intestinal lumen may trigger inflammatory responses, inducing the phosphorylation of serine residues in insulin receptor substrate-1, reducing insulin sensitivity. In type 1 diabetes, the lowered expression of adhesion proteins within the intestinal epithelium favours a greater immune response that may result in destruction of pancreatic β cells by CD8+ T-lymphocytes, and increased expression of interleukin-17, related to autoimmunity. Research in animal models and humans has hypothesized whether the administration of probiotics may improve the prognosis of diabetes through modulation of gut microbiota. We have shown in this review that a large body of evidence suggests probiotics reduce the inflammatory response and oxidative stress, as well as increase the expression of adhesion proteins within the intestinal epithelium, reducing intestinal permeability. Such effects increase insulin sensitivity and reduce autoimmune response. However, further investigations are required to clarify whether the administration of probiotics can be efficiently used for the prevention and management of diabetes.</abstract><cop>England</cop><pub>Springer-Verlag</pub><pmid>24939063</pmid><doi>10.1186/1475-2891-13-60</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1475-2891 |
| ispartof | Nutrition journal, 2014-06, Vol.13 (1), p.60-60, Article 60 |
| issn | 1475-2891 1475-2891 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4078018 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central Open Access; Springer Nature OA Free Journals; Springer Nature - Complete Springer Journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | adhesion Analysis animal models Animals autoimmunity Care and treatment CD8-positive T-lymphocytes Clinical Trials as Topic Development and progression Diabetes Mellitus, Type 1 - etiology Diabetes Mellitus, Type 1 - therapy Diabetes Mellitus, Type 2 - etiology Diabetes Mellitus, Type 2 - therapy Fatty acids Gastrointestinal Tract - microbiology Humans Immune response Inflammation Inflammation - etiology Insulin insulin receptors Insulin Resistance insulin-dependent diabetes mellitus Interleukins intestinal microorganisms intestinal mucosa Kinases laboratory animals Lymphocytes Metabolic disorders Microbiota noninsulin-dependent diabetes mellitus Nutrition oxidative stress Pancreatic beta cells Patient outcomes permeability phosphorylation Probiotics Probiotics - therapeutic use prognosis Review serine Studies Toll-Like Receptor 4 - physiology Type 2 diabetes |
| title | Gut microbiota, probiotics and diabetes |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-16T03%3A34%3A48IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Gut%20microbiota,%20probiotics%20and%20diabetes&rft.jtitle=Nutrition%20journal&rft.au=Gomes,%20Aline%20Corado&rft.date=2014-06-17&rft.volume=13&rft.issue=1&rft.spage=60&rft.epage=60&rft.pages=60-60&rft.artnum=60&rft.issn=1475-2891&rft.eissn=1475-2891&rft_id=info:doi/10.1186/1475-2891-13-60&rft_dat=%3Cgale_pubme%3EA539675915%3C/gale_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1542264171&rft_id=info:pmid/24939063&rft_galeid=A539675915&rfr_iscdi=true |