Intestinal Ralstonia pickettii augments glucose intolerance in obesity
An altered intestinal microbiota composition has been implicated in the pathogenesis of metabolic disease including obesity and type 2 diabetes mellitus (T2DM). Low grade inflammation, potentially initiated by the intestinal microbiota, has been suggested to be a driving force in the development of...
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| Veröffentlicht in: | PloS one 2017-11, Vol.12 (11), p.e0181693-e0181693 |
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| creator | Udayappan, Shanthadevi D Kovatcheva-Datchary, Petia Bakker, Guido J Havik, Stefan R Herrema, Hilde Cani, Patrice D Bouter, Kristien E Belzer, Clara Witjes, Julia J Vrieze, Anne de Sonnaville, Noor Chaplin, Alice van Raalte, Daniel H Aalvink, Steven Dallinga-Thie, Geesje M Heilig, Hans G H J Bergström, Göran van der Meij, Suzan van Wagensveld, Bart A Hoekstra, Joost B L Holleman, Frits Stroes, Erik S G Groen, Albert K Bäckhed, Fredrik de Vos, Willem M Nieuwdorp, Max |
| description | An altered intestinal microbiota composition has been implicated in the pathogenesis of metabolic disease including obesity and type 2 diabetes mellitus (T2DM). Low grade inflammation, potentially initiated by the intestinal microbiota, has been suggested to be a driving force in the development of insulin resistance in obesity. Here, we report that bacterial DNA is present in mesenteric adipose tissue of obese but otherwise healthy human subjects. Pyrosequencing of bacterial 16S rRNA genes revealed that DNA from the Gram-negative species Ralstonia was most prevalent. Interestingly, fecal abundance of Ralstonia pickettii was increased in obese subjects with pre-diabetes and T2DM. To assess if R. pickettii was causally involved in development of obesity and T2DM, we performed a proof-of-concept study in diet-induced obese (DIO) mice. Compared to vehicle-treated control mice, R. pickettii-treated DIO mice had reduced glucose tolerance. In addition, circulating levels of endotoxin were increased in R. pickettii-treated mice. In conclusion, this study suggests that intestinal Ralstonia is increased in obese human subjects with T2DM and reciprocally worsens glucose tolerance in DIO mice. |
| doi_str_mv | 10.1371/journal.pone.0181693 |
| format | Article |
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Low grade inflammation, potentially initiated by the intestinal microbiota, has been suggested to be a driving force in the development of insulin resistance in obesity. Here, we report that bacterial DNA is present in mesenteric adipose tissue of obese but otherwise healthy human subjects. Pyrosequencing of bacterial 16S rRNA genes revealed that DNA from the Gram-negative species Ralstonia was most prevalent. Interestingly, fecal abundance of Ralstonia pickettii was increased in obese subjects with pre-diabetes and T2DM. To assess if R. pickettii was causally involved in development of obesity and T2DM, we performed a proof-of-concept study in diet-induced obese (DIO) mice. Compared to vehicle-treated control mice, R. pickettii-treated DIO mice had reduced glucose tolerance. In addition, circulating levels of endotoxin were increased in R. pickettii-treated mice. In conclusion, this study suggests that intestinal Ralstonia is increased in obese human subjects with T2DM and reciprocally worsens glucose tolerance in DIO mice.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0181693</identifier><identifier>PMID: 29166392</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adipose tissue ; Aged ; Animals ; Bacteria ; Biology and Life Sciences ; Deoxyribonucleic acid ; Development and progression ; Diabetes ; Diabetes mellitus ; Diabetes Mellitus, Type 2 - complications ; Diabetes Mellitus, Type 2 - microbiology ; Diet, High-Fat ; diet-induced obesity ; DNA ; DNA, Bacterial - analysis ; Endocrinology and Diabetes ; Endokrinologi och diabetes ; Endotoxins ; fat ; Feces - microbiology ; Female ; gastrointestinal-tract ; Glucose ; Glucose intolerance ; Glucose Intolerance - complications ; Glucose Intolerance - microbiology ; Glucose tolerance ; Gram-Negative Bacterial Infections - microbiology ; Gram-Negative Bacterial Infections - pathology ; gut microbiota ; Humans ; immunity ; Inflammation - complications ; Inflammation - pathology ; Insulin ; Insulin resistance ; Intestinal microflora ; Intestine ; Intestines - microbiology ; Intestines - pathology ; Intolerance ; Intra-Abdominal Fat - microbiology ; Intra-Abdominal Fat - pathology ; Laboratorium voor Microbiologie ; low-grade inflammation ; Male ; Medicine and Health Sciences ; Metabolic diseases ; Metabolic disorders ; metabolic syndrome ; Mice ; Mice, Inbred C57BL ; Microbiological Laboratory ; Microbiologie ; Microbiology ; Microbiota ; Microbiota (Symbiotic organisms) ; Obesity ; Obesity - complications ; Obesity - microbiology ; Pathogenesis ; Physical sciences ; Physiological aspects ; Ralstonia pickettii ; Ralstonia pickettii - physiology ; receptor 5 ; Risk factors ; Rodents ; rRNA 16S ; Soil bacteria ; Teaching hospitals ; VLAG ; WIMEK</subject><ispartof>PloS one, 2017-11, Vol.12 (11), p.e0181693-e0181693</ispartof><rights>COPYRIGHT 2017 Public Library of Science</rights><rights>2017 Udayappan et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. 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Low grade inflammation, potentially initiated by the intestinal microbiota, has been suggested to be a driving force in the development of insulin resistance in obesity. Here, we report that bacterial DNA is present in mesenteric adipose tissue of obese but otherwise healthy human subjects. Pyrosequencing of bacterial 16S rRNA genes revealed that DNA from the Gram-negative species Ralstonia was most prevalent. Interestingly, fecal abundance of Ralstonia pickettii was increased in obese subjects with pre-diabetes and T2DM. To assess if R. pickettii was causally involved in development of obesity and T2DM, we performed a proof-of-concept study in diet-induced obese (DIO) mice. Compared to vehicle-treated control mice, R. pickettii-treated DIO mice had reduced glucose tolerance. In addition, circulating levels of endotoxin were increased in R. pickettii-treated mice. In conclusion, this study suggests that intestinal Ralstonia is increased in obese human subjects with T2DM and reciprocally worsens glucose tolerance in DIO mice.</description><subject>Adipose tissue</subject><subject>Aged</subject><subject>Animals</subject><subject>Bacteria</subject><subject>Biology and Life Sciences</subject><subject>Deoxyribonucleic acid</subject><subject>Development and progression</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Type 2 - complications</subject><subject>Diabetes Mellitus, Type 2 - microbiology</subject><subject>Diet, High-Fat</subject><subject>diet-induced obesity</subject><subject>DNA</subject><subject>DNA, Bacterial - analysis</subject><subject>Endocrinology and Diabetes</subject><subject>Endokrinologi och diabetes</subject><subject>Endotoxins</subject><subject>fat</subject><subject>Feces - microbiology</subject><subject>Female</subject><subject>gastrointestinal-tract</subject><subject>Glucose</subject><subject>Glucose intolerance</subject><subject>Glucose Intolerance - complications</subject><subject>Glucose Intolerance - microbiology</subject><subject>Glucose tolerance</subject><subject>Gram-Negative Bacterial Infections - microbiology</subject><subject>Gram-Negative Bacterial Infections - pathology</subject><subject>gut microbiota</subject><subject>Humans</subject><subject>immunity</subject><subject>Inflammation - complications</subject><subject>Inflammation - pathology</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Intestinal microflora</subject><subject>Intestine</subject><subject>Intestines - microbiology</subject><subject>Intestines - pathology</subject><subject>Intolerance</subject><subject>Intra-Abdominal Fat - microbiology</subject><subject>Intra-Abdominal Fat - pathology</subject><subject>Laboratorium voor Microbiologie</subject><subject>low-grade inflammation</subject><subject>Male</subject><subject>Medicine and Health Sciences</subject><subject>Metabolic diseases</subject><subject>Metabolic disorders</subject><subject>metabolic syndrome</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Microbiological Laboratory</subject><subject>Microbiologie</subject><subject>Microbiology</subject><subject>Microbiota</subject><subject>Microbiota (Symbiotic organisms)</subject><subject>Obesity</subject><subject>Obesity - complications</subject><subject>Obesity - microbiology</subject><subject>Pathogenesis</subject><subject>Physical sciences</subject><subject>Physiological aspects</subject><subject>Ralstonia pickettii</subject><subject>Ralstonia pickettii - physiology</subject><subject>receptor 5</subject><subject>Risk factors</subject><subject>Rodents</subject><subject>rRNA 16S</subject><subject>Soil bacteria</subject><subject>Teaching hospitals</subject><subject>VLAG</subject><subject>WIMEK</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNk-9r1DAcxosobk7_A9EDQfTFnfnRpKkvhDGcHgwG88fbkKZpL2cu6ZLUc_-96dqNq-yFFJrwzed50jzpN8teQrCCuIAftq73VphV56xaAcggLfGj7BiWGC0pAvjxwfwoexbCFgCCGaVPsyNUQkpxiY6z87WNKkSdnBZXwoTorBaLTstfKkatF6Jvd8rGsGhNL11QC22jM8oLK4f5wlUq6HjzPHvSJLV6MY0n2Y_zz9_Pvi4vLr-sz04vlrJgMC4ZyVFFCMsBAYrKCjSwRpBhUdQM4bICZVNJCRFmWAJM6ipVEKBFJYDAFAp8kr0efTvjAp8iCByWtMBFjkqQiPVI1E5seef1Tvgb7oTmtwXnWy581NIozmAum1rVhNImRyTtonJMqryui5wpTJPXx9FrL1pltU0vboWXOtwaGl35wXzfe27NMHR9FTjBIMdFEi9HcdirVJ99Stt3PJXangfFEYV5MfCfpqP11U7VMqXuhZnJ5itWb3jrfnNCy5JBnAzeTQbeXffpUvlOB6mMEVa5fgyJUVTAPKFv_kEfjnKiWpHS0rZxaV85mPJTAgnGkDGWqNUDVHpqtdMy_ZyNTvWZ4P1MkJio_sRW9CHw9ber_2cvf87ZtwfsRgkTN8GZPmpnwxzMR1B6F4JXzX3IEPCht-7S4ENv8am3kuzV4QXdi-6aCf8FaYYgZQ</recordid><startdate>20171122</startdate><enddate>20171122</enddate><creator>Udayappan, 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Ralstonia pickettii augments glucose intolerance in obesity</title><author>Udayappan, Shanthadevi D ; Kovatcheva-Datchary, Petia ; Bakker, Guido J ; Havik, Stefan R ; Herrema, Hilde ; Cani, Patrice D ; Bouter, Kristien E ; Belzer, Clara ; Witjes, Julia J ; Vrieze, Anne ; de Sonnaville, Noor ; Chaplin, Alice ; van Raalte, Daniel H ; Aalvink, Steven ; Dallinga-Thie, Geesje M ; Heilig, Hans G H J ; Bergström, Göran ; van der Meij, Suzan ; van Wagensveld, Bart A ; Hoekstra, Joost B L ; Holleman, Frits ; Stroes, Erik S G ; Groen, Albert K ; Bäckhed, Fredrik ; de Vos, Willem M ; Nieuwdorp, Max</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c781t-8542b5584050e6cb0f1d2183a7d8239b09fbcc12383c035dbb092067ba0a361a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adipose tissue</topic><topic>Aged</topic><topic>Animals</topic><topic>Bacteria</topic><topic>Biology and Life Sciences</topic><topic>Deoxyribonucleic acid</topic><topic>Development and progression</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes Mellitus, Type 2 - complications</topic><topic>Diabetes Mellitus, Type 2 - microbiology</topic><topic>Diet, High-Fat</topic><topic>diet-induced obesity</topic><topic>DNA</topic><topic>DNA, Bacterial - analysis</topic><topic>Endocrinology and Diabetes</topic><topic>Endokrinologi och diabetes</topic><topic>Endotoxins</topic><topic>fat</topic><topic>Feces - microbiology</topic><topic>Female</topic><topic>gastrointestinal-tract</topic><topic>Glucose</topic><topic>Glucose intolerance</topic><topic>Glucose Intolerance - complications</topic><topic>Glucose Intolerance - microbiology</topic><topic>Glucose tolerance</topic><topic>Gram-Negative Bacterial Infections - microbiology</topic><topic>Gram-Negative Bacterial Infections - pathology</topic><topic>gut 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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>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Göteborgs universitet</collection><collection>NARCIS:Publications</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Udayappan, Shanthadevi D</au><au>Kovatcheva-Datchary, Petia</au><au>Bakker, Guido J</au><au>Havik, Stefan R</au><au>Herrema, Hilde</au><au>Cani, Patrice D</au><au>Bouter, Kristien E</au><au>Belzer, Clara</au><au>Witjes, Julia J</au><au>Vrieze, Anne</au><au>de Sonnaville, Noor</au><au>Chaplin, Alice</au><au>van Raalte, Daniel H</au><au>Aalvink, Steven</au><au>Dallinga-Thie, Geesje M</au><au>Heilig, Hans G H J</au><au>Bergström, Göran</au><au>van der Meij, Suzan</au><au>van Wagensveld, Bart A</au><au>Hoekstra, Joost B L</au><au>Holleman, Frits</au><au>Stroes, Erik S G</au><au>Groen, Albert K</au><au>Bäckhed, Fredrik</au><au>de Vos, Willem M</au><au>Nieuwdorp, Max</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Intestinal Ralstonia pickettii augments glucose intolerance in obesity</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2017-11-22</date><risdate>2017</risdate><volume>12</volume><issue>11</issue><spage>e0181693</spage><epage>e0181693</epage><pages>e0181693-e0181693</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>An altered intestinal microbiota composition has been implicated in the pathogenesis of metabolic disease including obesity and type 2 diabetes mellitus (T2DM). Low grade inflammation, potentially initiated by the intestinal microbiota, has been suggested to be a driving force in the development of insulin resistance in obesity. Here, we report that bacterial DNA is present in mesenteric adipose tissue of obese but otherwise healthy human subjects. Pyrosequencing of bacterial 16S rRNA genes revealed that DNA from the Gram-negative species Ralstonia was most prevalent. Interestingly, fecal abundance of Ralstonia pickettii was increased in obese subjects with pre-diabetes and T2DM. To assess if R. pickettii was causally involved in development of obesity and T2DM, we performed a proof-of-concept study in diet-induced obese (DIO) mice. Compared to vehicle-treated control mice, R. pickettii-treated DIO mice had reduced glucose tolerance. In addition, circulating levels of endotoxin were increased in R. pickettii-treated mice. In conclusion, this study suggests that intestinal Ralstonia is increased in obese human subjects with T2DM and reciprocally worsens glucose tolerance in DIO mice.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>29166392</pmid><doi>10.1371/journal.pone.0181693</doi><tpages>e0181693</tpages><orcidid>https://orcid.org/0000-0002-0112-6348</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2017-11, Vol.12 (11), p.e0181693-e0181693 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1967374290 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | Adipose tissue Aged Animals Bacteria Biology and Life Sciences Deoxyribonucleic acid Development and progression Diabetes Diabetes mellitus Diabetes Mellitus, Type 2 - complications Diabetes Mellitus, Type 2 - microbiology Diet, High-Fat diet-induced obesity DNA DNA, Bacterial - analysis Endocrinology and Diabetes Endokrinologi och diabetes Endotoxins fat Feces - microbiology Female gastrointestinal-tract Glucose Glucose intolerance Glucose Intolerance - complications Glucose Intolerance - microbiology Glucose tolerance Gram-Negative Bacterial Infections - microbiology Gram-Negative Bacterial Infections - pathology gut microbiota Humans immunity Inflammation - complications Inflammation - pathology Insulin Insulin resistance Intestinal microflora Intestine Intestines - microbiology Intestines - pathology Intolerance Intra-Abdominal Fat - microbiology Intra-Abdominal Fat - pathology Laboratorium voor Microbiologie low-grade inflammation Male Medicine and Health Sciences Metabolic diseases Metabolic disorders metabolic syndrome Mice Mice, Inbred C57BL Microbiological Laboratory Microbiologie Microbiology Microbiota Microbiota (Symbiotic organisms) Obesity Obesity - complications Obesity - microbiology Pathogenesis Physical sciences Physiological aspects Ralstonia pickettii Ralstonia pickettii - physiology receptor 5 Risk factors Rodents rRNA 16S Soil bacteria Teaching hospitals VLAG WIMEK |
| title | Intestinal Ralstonia pickettii augments glucose intolerance in obesity |
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