Human intestinal microbiota composition is associated with local and systemic inflammation in obesity
Objective Intestinal microbiota have been suggested to contribute to the development of obesity, but the mechanism remains elusive. The relationship between microbiota composition, intestinal permeability, and inflammation in nonobese and obese subjects was investigated. Design and Methods Fecal mic...
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| Veröffentlicht in: | Obesity (Silver Spring, Md.) Jg. 21; H. 12; S. E607 - E615 |
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| Hauptverfasser: | , , , , , , , , |
| Format: | Journal Article |
| Sprache: | Englisch |
| Veröffentlicht: |
United States
Blackwell Publishing Ltd
01.12.2013
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| Schlagworte: | |
| ISSN: | 1930-7381, 1930-739X, 1930-739X |
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| Abstract | Objective
Intestinal microbiota have been suggested to contribute to the development of obesity, but the mechanism remains elusive. The relationship between microbiota composition, intestinal permeability, and inflammation in nonobese and obese subjects was investigated.
Design and Methods
Fecal microbiota composition of 28 subjects (BMI 18.6‐60.3 kg m−2) was analyzed by a phylogenetic profiling microarray. Fecal calprotectin and plasma C‐reactive protein levels were determined to evaluate intestinal and systemic inflammation. Furthermore, HbA1c, and plasma levels of transaminases and lipids were analyzed. Gastroduodenal, small intestinal, and colonic permeability were assessed by a multisaccharide test.
Results
Based on microbiota composition, the study population segregated into two clusters with predominantly obese (15/19) or exclusively nonobese (9/9) subjects. Whereas intestinal permeability did not differ between clusters, the obese cluster showed reduced bacterial diversity, a decreased Bacteroidetes/Firmicutes ratio, and an increased abundance of potential proinflammatory Proteobacteria. Interestingly, fecal calprotectin was only detectable in subjects within the obese microbiota cluster (n = 8/19, P = 0.02). Plasma C‐reactive protein was also increased in these subjects (P = 0.0005), and correlated with the Bacteroidetes/Firmicutes ratio (rs = −0.41, P = 0.03).
Conclusions
Intestinal microbiota alterations in obese subjects are associated with local and systemic inflammation, suggesting that the obesity‐related microbiota composition has a proinflammatory effect. |
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| AbstractList | OBJECTIVE: Intestinal microbiota have been suggested to contribute to the development of obesity, but the mechanism remains elusive. The relationship between microbiota composition, intestinal permeability, and inflammation in nonobese and obese subjects was investigated. DESIGN AND METHODS: Fecal microbiota composition of 28 subjects (BMI 18.6-60.3 kg m-2 ) was analyzed by a phylogenetic profiling microarray. Fecal calprotectin and plasma C-reactive protein levels were determined to evaluate intestinal and systemic inflammation. Furthermore, HbA1c , and plasma levels of transaminases and lipids were analyzed. Gastroduodenal, small intestinal, and colonic permeability were assessed by a multisaccharide test. RESULTS: Based on microbiota composition, the study population segregated into two clusters with predominantly obese (15/19) or exclusively nonobese (9/9) subjects. Whereas intestinal permeability did not differ between clusters, the obese cluster showed reduced bacterial diversity, a decreased Bacteroidetes/Firmicutes ratio, and an increased abundance of potential proinflammatory Proteobacteria. Interestingly, fecal calprotectin was only detectable in subjects within the obese microbiota cluster (n = 8/19, P = 0.02). Plasma C-reactive protein was also increased in these subjects (P = 0.0005), and correlated with the Bacteroidetes/Firmicutes ratio (rs = -0.41, P = 0.03). CONCLUSIONS: Intestinal microbiota alterations in obese subjects are associated with local and systemic inflammation, suggesting that the obesity-related microbiota composition has a proinflammatory effect Intestinal microbiota have been suggested to contribute to the development of obesity, but the mechanism remains elusive. The relationship between microbiota composition, intestinal permeability, and inflammation in nonobese and obese subjects was investigated. Fecal microbiota composition of 28 subjects (BMI 18.6-60.3 kg m^sup -2^) was analyzed by a phylogenetic profiling microarray. Fecal calprotectin and plasma C-reactive protein levels were determined to evaluate intestinal and systemic inflammation. Furthermore, HbA^sub 1c^, and plasma levels of transaminases and lipids were analyzed. Gastroduodenal, small intestinal, and colonic permeability were assessed by a multisaccharide test. Based on microbiota composition, the study population segregated into two clusters with predominantly obese (15/19) or exclusively nonobese (9/9) subjects. Whereas intestinal permeability did not differ between clusters, the obese cluster showed reduced bacterial diversity, a decreased Bacteroidetes/Firmicutes ratio, and an increased abundance of potential proinflammatory Proteobacteria. Interestingly, fecal calprotectin was only detectable in subjects within the obese microbiota cluster (n = 8/19, P = 0.02). Plasma C-reactive protein was also increased in these subjects ( P = 0.0005), and correlated with the Bacteroidetes/Firmicutes ratio (r^sub s^ = -0.41, P = 0.03). Intestinal microbiota alterations in obese subjects are associated with local and systemic inflammation, suggesting that the obesity-related microbiota composition has a proinflammatory effect. Intestinal microbiota have been suggested to contribute to the development of obesity, but the mechanism remains elusive. The relationship between microbiota composition, intestinal permeability, and inflammation in nonobese and obese subjects was investigated.OBJECTIVEIntestinal microbiota have been suggested to contribute to the development of obesity, but the mechanism remains elusive. The relationship between microbiota composition, intestinal permeability, and inflammation in nonobese and obese subjects was investigated.Fecal microbiota composition of 28 subjects (BMI 18.6-60.3 kg m(-2) ) was analyzed by a phylogenetic profiling microarray. Fecal calprotectin and plasma C-reactive protein levels were determined to evaluate intestinal and systemic inflammation. Furthermore, HbA1c , and plasma levels of transaminases and lipids were analyzed. Gastroduodenal, small intestinal, and colonic permeability were assessed by a multisaccharide test.DESIGN AND METHODSFecal microbiota composition of 28 subjects (BMI 18.6-60.3 kg m(-2) ) was analyzed by a phylogenetic profiling microarray. Fecal calprotectin and plasma C-reactive protein levels were determined to evaluate intestinal and systemic inflammation. Furthermore, HbA1c , and plasma levels of transaminases and lipids were analyzed. Gastroduodenal, small intestinal, and colonic permeability were assessed by a multisaccharide test.Based on microbiota composition, the study population segregated into two clusters with predominantly obese (15/19) or exclusively nonobese (9/9) subjects. Whereas intestinal permeability did not differ between clusters, the obese cluster showed reduced bacterial diversity, a decreased Bacteroidetes/Firmicutes ratio, and an increased abundance of potential proinflammatory Proteobacteria. Interestingly, fecal calprotectin was only detectable in subjects within the obese microbiota cluster (n = 8/19, P = 0.02). Plasma C-reactive protein was also increased in these subjects (P = 0.0005), and correlated with the Bacteroidetes/Firmicutes ratio (rs = -0.41, P = 0.03).RESULTSBased on microbiota composition, the study population segregated into two clusters with predominantly obese (15/19) or exclusively nonobese (9/9) subjects. Whereas intestinal permeability did not differ between clusters, the obese cluster showed reduced bacterial diversity, a decreased Bacteroidetes/Firmicutes ratio, and an increased abundance of potential proinflammatory Proteobacteria. Interestingly, fecal calprotectin was only detectable in subjects within the obese microbiota cluster (n = 8/19, P = 0.02). Plasma C-reactive protein was also increased in these subjects (P = 0.0005), and correlated with the Bacteroidetes/Firmicutes ratio (rs = -0.41, P = 0.03).Intestinal microbiota alterations in obese subjects are associated with local and systemic inflammation, suggesting that the obesity-related microbiota composition has a proinflammatory effect.CONCLUSIONSIntestinal microbiota alterations in obese subjects are associated with local and systemic inflammation, suggesting that the obesity-related microbiota composition has a proinflammatory effect. Objective Intestinal microbiota have been suggested to contribute to the development of obesity, but the mechanism remains elusive. The relationship between microbiota composition, intestinal permeability, and inflammation in nonobese and obese subjects was investigated. Design and Methods Fecal microbiota composition of 28 subjects (BMI 18.6‐60.3 kg m−2) was analyzed by a phylogenetic profiling microarray. Fecal calprotectin and plasma C‐reactive protein levels were determined to evaluate intestinal and systemic inflammation. Furthermore, HbA1c, and plasma levels of transaminases and lipids were analyzed. Gastroduodenal, small intestinal, and colonic permeability were assessed by a multisaccharide test. Results Based on microbiota composition, the study population segregated into two clusters with predominantly obese (15/19) or exclusively nonobese (9/9) subjects. Whereas intestinal permeability did not differ between clusters, the obese cluster showed reduced bacterial diversity, a decreased Bacteroidetes/Firmicutes ratio, and an increased abundance of potential proinflammatory Proteobacteria. Interestingly, fecal calprotectin was only detectable in subjects within the obese microbiota cluster (n = 8/19, P = 0.02). Plasma C‐reactive protein was also increased in these subjects (P = 0.0005), and correlated with the Bacteroidetes/Firmicutes ratio (rs = −0.41, P = 0.03). Conclusions Intestinal microbiota alterations in obese subjects are associated with local and systemic inflammation, suggesting that the obesity‐related microbiota composition has a proinflammatory effect. Intestinal microbiota have been suggested to contribute to the development of obesity, but the mechanism remains elusive. The relationship between microbiota composition, intestinal permeability, and inflammation in nonobese and obese subjects was investigated. Fecal microbiota composition of 28 subjects (BMI 18.6-60.3 kg m(-2) ) was analyzed by a phylogenetic profiling microarray. Fecal calprotectin and plasma C-reactive protein levels were determined to evaluate intestinal and systemic inflammation. Furthermore, HbA1c , and plasma levels of transaminases and lipids were analyzed. Gastroduodenal, small intestinal, and colonic permeability were assessed by a multisaccharide test. Based on microbiota composition, the study population segregated into two clusters with predominantly obese (15/19) or exclusively nonobese (9/9) subjects. Whereas intestinal permeability did not differ between clusters, the obese cluster showed reduced bacterial diversity, a decreased Bacteroidetes/Firmicutes ratio, and an increased abundance of potential proinflammatory Proteobacteria. Interestingly, fecal calprotectin was only detectable in subjects within the obese microbiota cluster (n = 8/19, P = 0.02). Plasma C-reactive protein was also increased in these subjects (P = 0.0005), and correlated with the Bacteroidetes/Firmicutes ratio (rs = -0.41, P = 0.03). Intestinal microbiota alterations in obese subjects are associated with local and systemic inflammation, suggesting that the obesity-related microbiota composition has a proinflammatory effect. |
| Author | Buurman, Wim A. de Vos, Willem M. Zoetendal, Erwin G. Verdam, Froukje J. de Jonge, Charlotte Erbil, Runi Fuentes, Susana Greve, Jan Willem Rensen, Sander S. |
| Author_xml | – sequence: 1 givenname: Froukje J. surname: Verdam fullname: Verdam, Froukje J. organization: Atrium Medical Center Parkstad – sequence: 2 givenname: Susana surname: Fuentes fullname: Fuentes, Susana organization: Wageningen University – sequence: 3 givenname: Charlotte surname: de Jonge fullname: de Jonge, Charlotte organization: Atrium Medical Center Parkstad – sequence: 4 givenname: Erwin G. surname: Zoetendal fullname: Zoetendal, Erwin G. organization: Wageningen University – sequence: 5 givenname: Runi surname: Erbil fullname: Erbil, Runi organization: Maastricht University Medical Center – sequence: 6 givenname: Jan Willem surname: Greve fullname: Greve, Jan Willem organization: Atrium Medical Center Parkstad – sequence: 7 givenname: Wim A. surname: Buurman fullname: Buurman, Wim A. organization: Maastricht University Medical Center – sequence: 8 givenname: Willem M. surname: de Vos fullname: de Vos, Willem M. organization: Wageningen University – sequence: 9 givenname: Sander S. surname: Rensen fullname: Rensen, Sander S. organization: Maastricht University Medical Center |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23526699$$D View this record in MEDLINE/PubMed |
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| Notes | All authors hereby declare they have no competing financial interests in relation to the work described here. FJV, CdJ, EGZ, JWG, WAB, WMDV, and SSR conceived the study. Data was collected by FJV, SF, CdJ, EGZ, and RE, analyzed by FJV, SF, EGZ, WAB, and SSR, and interpreted by FJV, SF, CdJ, EGZ, JWG, WAB, WMDV, and SSR. Literature searches were performed by FJV, SF, EGZ, JWG, WAB, WMDV, and SSR. Figures were generated by FJV, SF, and SSR. All authors were involved in writing the article and had final approval of the submitted version. Disclosure Funding agencies This work was financially supported by a Senter Novem IOP genomics grant to WAB and JWG (IGE05012A), a Transnational University Limburg grant and a Dutch Digestive Foundation project grant (WO 09‐46) to SSR, and a Spinoza award to WMDV (NWO). Author contributions SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 14 ObjectType-Article-1 ObjectType-Feature-2 content type line 23 |
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| References | 2004; 101 2007; 104 2010; 32 2010; 59 2012; 486 2010; 13 2010; 107 2006; 12 2010; 18 2010; 104 2008; 32 2008; 105 2008; 6 2008; 3 2003 2010; 81 2011; 3 2009; 137 2009; 11 2011; 225 2009; 58 2013; 32 2009; 50 2005; 102 2006; 44 2007; 292 2010; 299 2004; 13 2012; 490 2008; 87 2011; 46 2011; 45 2009; 4 2009; 461 2008; 453 2010; 5 2012; 23 2011; 121 2006; 444 e_1_2_6_32_1 e_1_2_6_10_1 e_1_2_6_31_1 e_1_2_6_30_1 e_1_2_6_19_1 e_1_2_6_13_1 e_1_2_6_36_1 e_1_2_6_14_1 e_1_2_6_35_1 e_1_2_6_11_1 e_1_2_6_34_1 e_1_2_6_12_1 e_1_2_6_33_1 e_1_2_6_18_1 e_1_2_6_39_1 e_1_2_6_15_1 e_1_2_6_38_1 e_1_2_6_16_1 e_1_2_6_37_1 e_1_2_6_21_1 e_1_2_6_20_1 e_1_2_6_41_1 e_1_2_6_40_1 e_1_2_6_9_1 e_1_2_6_8_1 e_1_2_6_5_1 e_1_2_6_4_1 e_1_2_6_7_1 e_1_2_6_6_1 e_1_2_6_25_1 Sluijs Veer G (e_1_2_6_17_1) 2006; 44 e_1_2_6_24_1 e_1_2_6_3_1 e_1_2_6_23_1 e_1_2_6_2_1 e_1_2_6_22_1 e_1_2_6_29_1 e_1_2_6_28_1 e_1_2_6_27_1 e_1_2_6_26_1 |
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Intestinal microbiota have been suggested to contribute to the development of obesity, but the mechanism remains elusive. The relationship between... Intestinal microbiota have been suggested to contribute to the development of obesity, but the mechanism remains elusive. The relationship between microbiota... OBJECTIVE: Intestinal microbiota have been suggested to contribute to the development of obesity, but the mechanism remains elusive. The relationship between... |
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| SubjectTerms | Adult Age Body Mass Index bowel C-Reactive Protein - metabolism Comorbidity Deoxyribonucleic acid Diabetes diet-induced obesity disease DNA fecal calprotectin Feces - chemistry Feces - microbiology Female high-fat diet human gut microbiota Humans Inflammation - microbiology Insulin resistance Intestines - microbiology Leukocyte L1 Antigen Complex - metabolism Male Metabolic disorders mice Microbiota Middle Aged Multivariate analysis nonalcoholic steatohepatitis Nutrition research Obesity Obesity - microbiology Oligonucleotide Array Sequence Analysis Permeability Phylogenetics Studies Urine weight-loss Young Adult |
| Title | Human intestinal microbiota composition is associated with local and systemic inflammation in obesity |
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