Structural changes of gut microbiota during berberine-mediated prevention of obesity and insulin resistance in high-fat diet-fed rats
Berberine, a major pharmacological component of the Chinese herb Coptis chinensis, which was originally used to treat bacterial diarrhea, has recently been demonstrated to be clinically effective in alleviating type 2 diabetes. In this study, we revealed that berberine effectively prevented the deve...
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| Veröffentlicht in: | PloS one 2012-08, Vol.7 (8), p.e42529 |
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| creator | Zhang, Xu Zhao, Yufeng Zhang, Menghui Pang, Xiaoyan Xu, Jia Kang, Chaoying Li, Meng Zhang, Chenhong Zhang, Zhiguo Zhang, Yifei Li, Xiaoying Ning, Guang Zhao, Liping |
| description | Berberine, a major pharmacological component of the Chinese herb Coptis chinensis, which was originally used to treat bacterial diarrhea, has recently been demonstrated to be clinically effective in alleviating type 2 diabetes. In this study, we revealed that berberine effectively prevented the development of obesity and insulin resistance in high-fat diet (HFD)-fed rats, which showed decreased food intake. Increases in the levels of serum lipopolysaccharide-binding protein, monocyte chemoattractant protein-1, and leptin and decrease in the serum level of adiponectin corrected for body fat in HFD-fed rats were also significantly retarded by the co-administration of berberine at 100 mg/kg body weight. Bar-coded pyrosequencing of the V3 region of 16S rRNA genes revealed a significant reduction in the gut microbiota diversity of berberine-treated rats. UniFrac principal coordinates analysis revealed a marked shift of the gut microbiota structure in berberine-treated rats away from that of the controls. Redundancy analysis identified 268 berberine-responding operational taxonomic units (OTUs), most of which were essentially eliminated, whereas a few putative short-chain fatty acid (SCFA)-producing bacteria, including Blautia and Allobaculum, were selectively enriched, along with elevations of fecal SCFA concentrations. Partial least square regression models based on these 268 OTUs were established (Q(2)>0.6) for predicting the adiposity index, body weight, leptin and adiponectin corrected for body fat, indicating that these discrete phylotypes might have a close association with the host metabolic phenotypes. Taken together, our findings suggest that the prevention of obesity and insulin resistance by berberine in HFD-fed rats is at least partially mediated by structural modulation of the gut microbiota, which may help to alleviate inflammation by reducing the exogenous antigen load in the host and elevating SCFA levels in the intestine. |
| doi_str_mv | 10.1371/journal.pone.0042529 |
| format | Article |
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In this study, we revealed that berberine effectively prevented the development of obesity and insulin resistance in high-fat diet (HFD)-fed rats, which showed decreased food intake. Increases in the levels of serum lipopolysaccharide-binding protein, monocyte chemoattractant protein-1, and leptin and decrease in the serum level of adiponectin corrected for body fat in HFD-fed rats were also significantly retarded by the co-administration of berberine at 100 mg/kg body weight. Bar-coded pyrosequencing of the V3 region of 16S rRNA genes revealed a significant reduction in the gut microbiota diversity of berberine-treated rats. UniFrac principal coordinates analysis revealed a marked shift of the gut microbiota structure in berberine-treated rats away from that of the controls. Redundancy analysis identified 268 berberine-responding operational taxonomic units (OTUs), most of which were essentially eliminated, whereas a few putative short-chain fatty acid (SCFA)-producing bacteria, including Blautia and Allobaculum, were selectively enriched, along with elevations of fecal SCFA concentrations. Partial least square regression models based on these 268 OTUs were established (Q(2)>0.6) for predicting the adiposity index, body weight, leptin and adiponectin corrected for body fat, indicating that these discrete phylotypes might have a close association with the host metabolic phenotypes. Taken together, our findings suggest that the prevention of obesity and insulin resistance by berberine in HFD-fed rats is at least partially mediated by structural modulation of the gut microbiota, which may help to alleviate inflammation by reducing the exogenous antigen load in the host and elevating SCFA levels in the intestine.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0042529</identifier><identifier>PMID: 22880019</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adiponectin ; Adipose tissue ; Adiposity - drug effects ; Animals ; Berberine ; Berberine - pharmacology ; Berberine - therapeutic use ; Bioavailability ; Biology ; Biotechnology ; Body fat ; Body weight ; Chemistry ; Cholesterol ; Diabetes ; Diabetes mellitus ; Diabetes mellitus (non-insulin dependent) ; Diarrhea ; Diet ; Diet, High-Fat ; Digestive system ; Digestive tract ; Fatty acids ; Fatty Acids, Volatile - metabolism ; Feces - chemistry ; Feeding Behavior - drug effects ; Firmicutes ; Food intake ; Gastrointestinal tract ; Gastrointestinal Tract - drug effects ; Gastrointestinal Tract - microbiology ; Gene expression ; High fat diet ; Inflammation - complications ; Inflammation - pathology ; Insulin ; Insulin Resistance ; Intestinal microflora ; Intestine ; Kinases ; Laboratories ; Lactobacillus ; Least-Squares Analysis ; Leptin ; Life sciences ; Lipopolysaccharide-binding protein ; Lipoproteins ; Male ; Mathematical models ; Medicine ; Metabolic disorders ; Metagenome - drug effects ; Metagenome - genetics ; Microbiota ; Microbiota (Symbiotic organisms) ; Monocyte chemoattractant protein ; Monocyte chemoattractant protein 1 ; Obesity ; Obesity - complications ; Obesity - drug therapy ; Obesity - microbiology ; Obesity - prevention & control ; Pharmacology ; Phenotype ; Phylogeny ; Prevention ; Protein binding ; Proteins ; Rats ; Rats, Wistar ; Redundancy ; Regression analysis ; Regression models ; Rodents ; rRNA 16S ; Type 2 diabetes ; Weight control ; Weight Gain - drug effects</subject><ispartof>PloS one, 2012-08, Vol.7 (8), p.e42529</ispartof><rights>COPYRIGHT 2012 Public Library of Science</rights><rights>Zhang et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://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. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2012 Zhang et al 2012 Zhang et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c7249-f1c1db14300e0359fbc402dd3016ff973297bf7afd9401109a11c98f7efb78f83</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3411811/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3411811/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22880019$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Xu</creatorcontrib><creatorcontrib>Zhao, Yufeng</creatorcontrib><creatorcontrib>Zhang, Menghui</creatorcontrib><creatorcontrib>Pang, Xiaoyan</creatorcontrib><creatorcontrib>Xu, Jia</creatorcontrib><creatorcontrib>Kang, Chaoying</creatorcontrib><creatorcontrib>Li, Meng</creatorcontrib><creatorcontrib>Zhang, Chenhong</creatorcontrib><creatorcontrib>Zhang, Zhiguo</creatorcontrib><creatorcontrib>Zhang, Yifei</creatorcontrib><creatorcontrib>Li, Xiaoying</creatorcontrib><creatorcontrib>Ning, Guang</creatorcontrib><creatorcontrib>Zhao, Liping</creatorcontrib><title>Structural changes of gut microbiota during berberine-mediated prevention of obesity and insulin resistance in high-fat diet-fed rats</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Berberine, a major pharmacological component of the Chinese herb Coptis chinensis, which was originally used to treat bacterial diarrhea, has recently been demonstrated to be clinically effective in alleviating type 2 diabetes. In this study, we revealed that berberine effectively prevented the development of obesity and insulin resistance in high-fat diet (HFD)-fed rats, which showed decreased food intake. Increases in the levels of serum lipopolysaccharide-binding protein, monocyte chemoattractant protein-1, and leptin and decrease in the serum level of adiponectin corrected for body fat in HFD-fed rats were also significantly retarded by the co-administration of berberine at 100 mg/kg body weight. Bar-coded pyrosequencing of the V3 region of 16S rRNA genes revealed a significant reduction in the gut microbiota diversity of berberine-treated rats. UniFrac principal coordinates analysis revealed a marked shift of the gut microbiota structure in berberine-treated rats away from that of the controls. Redundancy analysis identified 268 berberine-responding operational taxonomic units (OTUs), most of which were essentially eliminated, whereas a few putative short-chain fatty acid (SCFA)-producing bacteria, including Blautia and Allobaculum, were selectively enriched, along with elevations of fecal SCFA concentrations. Partial least square regression models based on these 268 OTUs were established (Q(2)>0.6) for predicting the adiposity index, body weight, leptin and adiponectin corrected for body fat, indicating that these discrete phylotypes might have a close association with the host metabolic phenotypes. Taken together, our findings suggest that the prevention of obesity and insulin resistance by berberine in HFD-fed rats is at least partially mediated by structural modulation of the gut microbiota, which may help to alleviate inflammation by reducing the exogenous antigen load in the host and elevating SCFA levels in the intestine.</description><subject>Adiponectin</subject><subject>Adipose tissue</subject><subject>Adiposity - drug effects</subject><subject>Animals</subject><subject>Berberine</subject><subject>Berberine - pharmacology</subject><subject>Berberine - therapeutic use</subject><subject>Bioavailability</subject><subject>Biology</subject><subject>Biotechnology</subject><subject>Body fat</subject><subject>Body weight</subject><subject>Chemistry</subject><subject>Cholesterol</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Diarrhea</subject><subject>Diet</subject><subject>Diet, High-Fat</subject><subject>Digestive system</subject><subject>Digestive tract</subject><subject>Fatty acids</subject><subject>Fatty Acids, Volatile - metabolism</subject><subject>Feces - chemistry</subject><subject>Feeding Behavior - drug effects</subject><subject>Firmicutes</subject><subject>Food intake</subject><subject>Gastrointestinal tract</subject><subject>Gastrointestinal Tract - drug effects</subject><subject>Gastrointestinal Tract - microbiology</subject><subject>Gene expression</subject><subject>High fat diet</subject><subject>Inflammation - complications</subject><subject>Inflammation - pathology</subject><subject>Insulin</subject><subject>Insulin Resistance</subject><subject>Intestinal microflora</subject><subject>Intestine</subject><subject>Kinases</subject><subject>Laboratories</subject><subject>Lactobacillus</subject><subject>Least-Squares Analysis</subject><subject>Leptin</subject><subject>Life sciences</subject><subject>Lipopolysaccharide-binding protein</subject><subject>Lipoproteins</subject><subject>Male</subject><subject>Mathematical models</subject><subject>Medicine</subject><subject>Metabolic disorders</subject><subject>Metagenome - drug effects</subject><subject>Metagenome - genetics</subject><subject>Microbiota</subject><subject>Microbiota (Symbiotic organisms)</subject><subject>Monocyte chemoattractant protein</subject><subject>Monocyte chemoattractant protein 1</subject><subject>Obesity</subject><subject>Obesity - complications</subject><subject>Obesity - drug therapy</subject><subject>Obesity - microbiology</subject><subject>Obesity - prevention & control</subject><subject>Pharmacology</subject><subject>Phenotype</subject><subject>Phylogeny</subject><subject>Prevention</subject><subject>Protein binding</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Redundancy</subject><subject>Regression analysis</subject><subject>Regression models</subject><subject>Rodents</subject><subject>rRNA 16S</subject><subject>Type 2 diabetes</subject><subject>Weight control</subject><subject>Weight Gain - drug effects</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNk2uL1DAUhoso7rr6D0QDguCHjrn0li8Ly-JlYGHBVb-GNJc2QycZc1ncH-D_NuN0lykoSAsNp8_7Jn17TlG8RHCFSIveb1zylk-rnbNqBWGFa0wfFaeIElw2GJLHR-uT4lkIGwhr0jXN0-IE466DENHT4tdN9EnE5PkExMjtoAJwGgwpgq0R3vXGRQ5k8sYOoFc-38aqcquk4VFJsPPqVtlonN3LXK-CiXeAWwmMDWkyFvhcCpFboXIJjGYYS80jkEbFUmcHz2N4XjzRfArqxfw8K759_PD18nN5df1pfXlxVYoWV7TUSCDZo4pAqCCpqe5FBbGUBKJGa9oSTNtet1xLWkGEIOUICdrpVum-7XRHzorXB9_d5AKbEwwMEdxg3NCaZGJ9IKTjG7bzZsv9HXPcsD8F5wfGfTRiUqyWEGqhYYdxX1GRd9ZSEyGUlD3HXZ29zufdUp8DEzmnHPPCdPnGmpEN7paRCqEOoWzwZjbw7kdSIf7jyDM18HwqY7XLZmJrgmAXdUVITqrZf_rqL1S-pMo_OveQNrm-ELxbCDIT1c848BQCW998-X_2-vuSfXvEjopPcQxuSvseCkuwOoC5DUPwSj8khyDbj8B9Gmw_AmwegSx7dZz6g-i-58lvDJUESQ</recordid><startdate>20120803</startdate><enddate>20120803</enddate><creator>Zhang, Xu</creator><creator>Zhao, Yufeng</creator><creator>Zhang, Menghui</creator><creator>Pang, Xiaoyan</creator><creator>Xu, Jia</creator><creator>Kang, Chaoying</creator><creator>Li, Meng</creator><creator>Zhang, Chenhong</creator><creator>Zhang, Zhiguo</creator><creator>Zhang, Yifei</creator><creator>Li, Xiaoying</creator><creator>Ning, Guang</creator><creator>Zhao, Liping</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20120803</creationdate><title>Structural changes of gut microbiota during berberine-mediated prevention of obesity and insulin resistance in high-fat diet-fed rats</title><author>Zhang, Xu ; Zhao, Yufeng ; Zhang, Menghui ; Pang, Xiaoyan ; Xu, Jia ; Kang, Chaoying ; Li, Meng ; Zhang, Chenhong ; Zhang, Zhiguo ; Zhang, Yifei ; Li, Xiaoying ; Ning, Guang ; Zhao, Liping</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c7249-f1c1db14300e0359fbc402dd3016ff973297bf7afd9401109a11c98f7efb78f83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adiponectin</topic><topic>Adipose tissue</topic><topic>Adiposity - 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pathology</topic><topic>Insulin</topic><topic>Insulin Resistance</topic><topic>Intestinal microflora</topic><topic>Intestine</topic><topic>Kinases</topic><topic>Laboratories</topic><topic>Lactobacillus</topic><topic>Least-Squares Analysis</topic><topic>Leptin</topic><topic>Life sciences</topic><topic>Lipopolysaccharide-binding protein</topic><topic>Lipoproteins</topic><topic>Male</topic><topic>Mathematical models</topic><topic>Medicine</topic><topic>Metabolic disorders</topic><topic>Metagenome - drug effects</topic><topic>Metagenome - genetics</topic><topic>Microbiota</topic><topic>Microbiota (Symbiotic organisms)</topic><topic>Monocyte chemoattractant protein</topic><topic>Monocyte chemoattractant protein 1</topic><topic>Obesity</topic><topic>Obesity - complications</topic><topic>Obesity - drug therapy</topic><topic>Obesity - microbiology</topic><topic>Obesity - prevention & control</topic><topic>Pharmacology</topic><topic>Phenotype</topic><topic>Phylogeny</topic><topic>Prevention</topic><topic>Protein binding</topic><topic>Proteins</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Redundancy</topic><topic>Regression analysis</topic><topic>Regression models</topic><topic>Rodents</topic><topic>rRNA 16S</topic><topic>Type 2 diabetes</topic><topic>Weight control</topic><topic>Weight Gain - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Xu</creatorcontrib><creatorcontrib>Zhao, Yufeng</creatorcontrib><creatorcontrib>Zhang, Menghui</creatorcontrib><creatorcontrib>Pang, Xiaoyan</creatorcontrib><creatorcontrib>Xu, Jia</creatorcontrib><creatorcontrib>Kang, Chaoying</creatorcontrib><creatorcontrib>Li, Meng</creatorcontrib><creatorcontrib>Zhang, Chenhong</creatorcontrib><creatorcontrib>Zhang, Zhiguo</creatorcontrib><creatorcontrib>Zhang, Yifei</creatorcontrib><creatorcontrib>Li, Xiaoying</creatorcontrib><creatorcontrib>Ning, Guang</creatorcontrib><creatorcontrib>Zhao, Liping</creatorcontrib><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: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</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>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</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>Zhang, Xu</au><au>Zhao, Yufeng</au><au>Zhang, Menghui</au><au>Pang, Xiaoyan</au><au>Xu, Jia</au><au>Kang, Chaoying</au><au>Li, Meng</au><au>Zhang, Chenhong</au><au>Zhang, Zhiguo</au><au>Zhang, Yifei</au><au>Li, Xiaoying</au><au>Ning, Guang</au><au>Zhao, Liping</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Structural changes of gut microbiota during berberine-mediated prevention of obesity and insulin resistance in high-fat diet-fed rats</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2012-08-03</date><risdate>2012</risdate><volume>7</volume><issue>8</issue><spage>e42529</spage><pages>e42529-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Berberine, a major pharmacological component of the Chinese herb Coptis chinensis, which was originally used to treat bacterial diarrhea, has recently been demonstrated to be clinically effective in alleviating type 2 diabetes. In this study, we revealed that berberine effectively prevented the development of obesity and insulin resistance in high-fat diet (HFD)-fed rats, which showed decreased food intake. Increases in the levels of serum lipopolysaccharide-binding protein, monocyte chemoattractant protein-1, and leptin and decrease in the serum level of adiponectin corrected for body fat in HFD-fed rats were also significantly retarded by the co-administration of berberine at 100 mg/kg body weight. Bar-coded pyrosequencing of the V3 region of 16S rRNA genes revealed a significant reduction in the gut microbiota diversity of berberine-treated rats. UniFrac principal coordinates analysis revealed a marked shift of the gut microbiota structure in berberine-treated rats away from that of the controls. Redundancy analysis identified 268 berberine-responding operational taxonomic units (OTUs), most of which were essentially eliminated, whereas a few putative short-chain fatty acid (SCFA)-producing bacteria, including Blautia and Allobaculum, were selectively enriched, along with elevations of fecal SCFA concentrations. Partial least square regression models based on these 268 OTUs were established (Q(2)>0.6) for predicting the adiposity index, body weight, leptin and adiponectin corrected for body fat, indicating that these discrete phylotypes might have a close association with the host metabolic phenotypes. Taken together, our findings suggest that the prevention of obesity and insulin resistance by berberine in HFD-fed rats is at least partially mediated by structural modulation of the gut microbiota, which may help to alleviate inflammation by reducing the exogenous antigen load in the host and elevating SCFA levels in the intestine.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>22880019</pmid><doi>10.1371/journal.pone.0042529</doi><tpages>e42529</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2012-08, Vol.7 (8), p.e42529 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1326226953 |
| 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 | Adiponectin Adipose tissue Adiposity - drug effects Animals Berberine Berberine - pharmacology Berberine - therapeutic use Bioavailability Biology Biotechnology Body fat Body weight Chemistry Cholesterol Diabetes Diabetes mellitus Diabetes mellitus (non-insulin dependent) Diarrhea Diet Diet, High-Fat Digestive system Digestive tract Fatty acids Fatty Acids, Volatile - metabolism Feces - chemistry Feeding Behavior - drug effects Firmicutes Food intake Gastrointestinal tract Gastrointestinal Tract - drug effects Gastrointestinal Tract - microbiology Gene expression High fat diet Inflammation - complications Inflammation - pathology Insulin Insulin Resistance Intestinal microflora Intestine Kinases Laboratories Lactobacillus Least-Squares Analysis Leptin Life sciences Lipopolysaccharide-binding protein Lipoproteins Male Mathematical models Medicine Metabolic disorders Metagenome - drug effects Metagenome - genetics Microbiota Microbiota (Symbiotic organisms) Monocyte chemoattractant protein Monocyte chemoattractant protein 1 Obesity Obesity - complications Obesity - drug therapy Obesity - microbiology Obesity - prevention & control Pharmacology Phenotype Phylogeny Prevention Protein binding Proteins Rats Rats, Wistar Redundancy Regression analysis Regression models Rodents rRNA 16S Type 2 diabetes Weight control Weight Gain - drug effects |
| title | Structural changes of gut microbiota during berberine-mediated prevention of obesity and insulin resistance in high-fat diet-fed rats |
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