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Gut-derived lipopolysaccharide augments adipose macrophage accumulation but is not essential for impaired glucose or insulin tolerance in mice

Background Obesity is associated with accumulation of macrophages in white adipose tissue (WAT), which contribute to the development of insulin resistance. Germ-free (GF) mice have reduced adiposity and are protected against diet-induced obesity, Objective To investigate whether the gut microbiota a... Full description

Journal Title: Gut 2012-12, Vol.61 (12), p.1701-1707
Main Author: Caesar, Robert
Other Authors: Reigstad, Christopher S , Bäckhed, Helene Kling , Reinhardt, Christoph , Ketonen, Maria , Östergren Lundén, Gunnel , Cani, Patrice D , Bäckhed, Fredrik
Format: Electronic Article Electronic Article
Language: English
Subjects:
lps
Publisher: London: BMJ Publishing Group Ltd and British Society of Gastroenterology
ID: ISSN: 0017-5749
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recordid: cdi_pubmed_primary_22535377
title: Gut-derived lipopolysaccharide augments adipose macrophage accumulation but is not essential for impaired glucose or insulin tolerance in mice
format: Article
creator:
  • Caesar, Robert
  • Reigstad, Christopher S
  • Bäckhed, Helene Kling
  • Reinhardt, Christoph
  • Ketonen, Maria
  • Östergren Lundén, Gunnel
  • Cani, Patrice D
  • Bäckhed, Fredrik
subjects:
  • 1506
  • Abridged Index Medicus
  • Adipose Tissue, White - immunology
  • Adipose Tissue, White - metabolism
  • Adipose Tissue, White - pathology
  • Animals
  • Biological and medical sciences
  • Biomarkers - metabolism
  • cardiovascular disease
  • colonic microflora
  • Diabetes. Impaired glucose tolerance
  • diet-induced obesity
  • E coli
  • Endocrine pancreas. Apud cells (diseases)
  • Endocrinopathies
  • endotoxemia
  • Endotoxin
  • energy metabolism
  • Escherichia
  • Escherichia coli - metabolism
  • escherichia-coli
  • Etiopathogenesis. Screening. Investigations. Target tissue resistance
  • Flow Cytometry
  • Gastroenterologi
  • Gastroenterology and Hepatology
  • Gastroenterology. Liver. Pancreas. Abdomen
  • Germ-Free Life
  • Glucose
  • Glucose intolerance
  • Glucose Intolerance - immunology
  • Glucose Intolerance - metabolism
  • Glucose Intolerance - microbiology
  • Glucose Intolerance - pathology
  • Glucose metabolism
  • gnotobiotic mice
  • gut microbiota
  • Immunoblotting
  • Immunohistochemistry
  • inflammation
  • Inflammation - immunology
  • Inflammation - metabolism
  • Inflammation - microbiology
  • Inflammation - pathology
  • inflammatory diseases
  • innate immunity
  • Insulin Resistance
  • intestinal epithelium
  • intestinal permeability
  • intestinal tract
  • Intestines - microbiology
  • Laboratories
  • lipid metabolism
  • lipids (amino acids
  • Lipopolysaccharides - metabolism
  • lps
  • Macrophages
  • Macrophages - metabolism
  • macrophages, obesity
  • Male
  • Medical sciences
  • Metabolic disorders
  • metabolic inflammation
  • metabolic inflammation, inflammation
  • Mice
  • microbiota
  • Microbiota (Symbiotic organisms)
  • modifications
  • mucosal immunity
  • Obesity
  • Original
  • Original Articles
  • peptides
  • prebiotic
  • proteins
  • resistance
  • Reverse Transcriptase Polymerase Chain Reaction
  • Rodents
  • tissue
  • toll-like receptors
ispartof: Gut, 2012-12, Vol.61 (12), p.1701-1707
description: Background Obesity is associated with accumulation of macrophages in white adipose tissue (WAT), which contribute to the development of insulin resistance. Germ-free (GF) mice have reduced adiposity and are protected against diet-induced obesity, Objective To investigate whether the gut microbiota and, specifically, gut-derived lipopolysaccharide (LPS) promote WAT inflammation and contribute to impaired glucose metabolism. Method Macrophage composition and expression of proinflammatory and anti-inflammatory markers were compared in WAT of GF, conventionally raised and Escherichia coli-monocolonised mice. Additionally, glucose and insulin tolerance in these mice was determined. Results The presence of a gut microbiota resulted in impaired glucose metabolism and increased macrophage accumulation and polarisation towards the proinflammatory M1 phenotype in WAT. Monocolonisation of GF mice for 4 weeks with E.coli W3110 or the isogenic strain MLK1067 (which expresses LPS with reduced immunogenicity) resulted in impaired glucose and insulin tolerance and promoted M1 polarisation of CD11b cells in WAT. However, colonisation with E.coli W3110 but not MLK1067 promoted macrophage accumulation and upregulation of proinflammatory and anti-inflammatory gene expression as well as JNK phosphorylation. Conclusion Gut microbiota induced LPS-dependent macrophage accumulation in WAT, whereas impairment of systemic glucose metabolism was not dependent on LPS. These results indicate that macrophage accumulation in WAT does not always correlate with impaired glucose metabolism.
language: eng
source:
identifier: ISSN: 0017-5749
fulltext: no_fulltext
issn:
  • 0017-5749
  • 1468-3288
url: Link


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titleGut-derived lipopolysaccharide augments adipose macrophage accumulation but is not essential for impaired glucose or insulin tolerance in mice
creatorCaesar, Robert ; Reigstad, Christopher S ; Bäckhed, Helene Kling ; Reinhardt, Christoph ; Ketonen, Maria ; Östergren Lundén, Gunnel ; Cani, Patrice D ; Bäckhed, Fredrik
creatorcontribCaesar, Robert ; Reigstad, Christopher S ; Bäckhed, Helene Kling ; Reinhardt, Christoph ; Ketonen, Maria ; Östergren Lundén, Gunnel ; Cani, Patrice D ; Bäckhed, Fredrik ; Wallenberg Laboratory ; Institute of Medicine, Department of Molecular and Clinical Medicine ; Göteborgs universitet ; Gothenburg University ; Sahlgrenska Academy ; Sahlgrenska akademin ; Wallenberglaboratoriet ; Institutionen för medicin, avdelningen för molekylär och klinisk medicin
descriptionBackground Obesity is associated with accumulation of macrophages in white adipose tissue (WAT), which contribute to the development of insulin resistance. Germ-free (GF) mice have reduced adiposity and are protected against diet-induced obesity, Objective To investigate whether the gut microbiota and, specifically, gut-derived lipopolysaccharide (LPS) promote WAT inflammation and contribute to impaired glucose metabolism. Method Macrophage composition and expression of proinflammatory and anti-inflammatory markers were compared in WAT of GF, conventionally raised and Escherichia coli-monocolonised mice. Additionally, glucose and insulin tolerance in these mice was determined. Results The presence of a gut microbiota resulted in impaired glucose metabolism and increased macrophage accumulation and polarisation towards the proinflammatory M1 phenotype in WAT. Monocolonisation of GF mice for 4 weeks with E.coli W3110 or the isogenic strain MLK1067 (which expresses LPS with reduced immunogenicity) resulted in impaired glucose and insulin tolerance and promoted M1 polarisation of CD11b cells in WAT. However, colonisation with E.coli W3110 but not MLK1067 promoted macrophage accumulation and upregulation of proinflammatory and anti-inflammatory gene expression as well as JNK phosphorylation. Conclusion Gut microbiota induced LPS-dependent macrophage accumulation in WAT, whereas impairment of systemic glucose metabolism was not dependent on LPS. These results indicate that macrophage accumulation in WAT does not always correlate with impaired glucose metabolism.
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publisherLondon: BMJ Publishing Group Ltd and British Society of Gastroenterology
subject1506 ; Abridged Index Medicus ; Adipose Tissue, White - immunology ; Adipose Tissue, White - metabolism ; Adipose Tissue, White - pathology ; Animals ; Biological and medical sciences ; Biomarkers - metabolism ; cardiovascular disease ; colonic microflora ; Diabetes. Impaired glucose tolerance ; diet-induced obesity ; E coli ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; endotoxemia ; Endotoxin ; energy metabolism ; Escherichia ; Escherichia coli - metabolism ; escherichia-coli ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Flow Cytometry ; Gastroenterologi ; Gastroenterology and Hepatology ; Gastroenterology. Liver. Pancreas. Abdomen ; Germ-Free Life ; Glucose ; Glucose intolerance ; Glucose Intolerance - immunology ; Glucose Intolerance - metabolism ; Glucose Intolerance - microbiology ; Glucose Intolerance - pathology ; Glucose metabolism ; gnotobiotic mice ; gut microbiota ; Immunoblotting ; Immunohistochemistry ; inflammation ; Inflammation - immunology ; Inflammation - metabolism ; Inflammation - microbiology ; Inflammation - pathology ; inflammatory diseases ; innate immunity ; Insulin Resistance ; intestinal epithelium ; intestinal permeability ; intestinal tract ; Intestines - microbiology ; Laboratories ; lipid metabolism ; lipids (amino acids ; Lipopolysaccharides - metabolism ; lps ; Macrophages ; Macrophages - metabolism ; macrophages, obesity ; Male ; Medical sciences ; Metabolic disorders ; metabolic inflammation ; metabolic inflammation, inflammation ; Mice ; microbiota ; Microbiota (Symbiotic organisms) ; modifications ; mucosal immunity ; Obesity ; Original ; Original Articles ; peptides ; prebiotic ; proteins ; resistance ; Reverse Transcriptase Polymerase Chain Reaction ; Rodents ; tissue ; toll-like receptors
ispartofGut, 2012-12, Vol.61 (12), p.1701-1707
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0Caesar, Robert
1Reigstad, Christopher S
2Bäckhed, Helene Kling
3Reinhardt, Christoph
4Ketonen, Maria
5Östergren Lundén, Gunnel
6Cani, Patrice D
7Bäckhed, Fredrik
8Wallenberg Laboratory
9Institute of Medicine, Department of Molecular and Clinical Medicine
10Göteborgs universitet
11Gothenburg University
12Sahlgrenska Academy
13Sahlgrenska akademin
14Wallenberglaboratoriet
15Institutionen för medicin, avdelningen för molekylär och klinisk medicin
title
0Gut-derived lipopolysaccharide augments adipose macrophage accumulation but is not essential for impaired glucose or insulin tolerance in mice
1Gut
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descriptionBackground Obesity is associated with accumulation of macrophages in white adipose tissue (WAT), which contribute to the development of insulin resistance. Germ-free (GF) mice have reduced adiposity and are protected against diet-induced obesity, Objective To investigate whether the gut microbiota and, specifically, gut-derived lipopolysaccharide (LPS) promote WAT inflammation and contribute to impaired glucose metabolism. Method Macrophage composition and expression of proinflammatory and anti-inflammatory markers were compared in WAT of GF, conventionally raised and Escherichia coli-monocolonised mice. Additionally, glucose and insulin tolerance in these mice was determined. Results The presence of a gut microbiota resulted in impaired glucose metabolism and increased macrophage accumulation and polarisation towards the proinflammatory M1 phenotype in WAT. Monocolonisation of GF mice for 4 weeks with E.coli W3110 or the isogenic strain MLK1067 (which expresses LPS with reduced immunogenicity) resulted in impaired glucose and insulin tolerance and promoted M1 polarisation of CD11b cells in WAT. However, colonisation with E.coli W3110 but not MLK1067 promoted macrophage accumulation and upregulation of proinflammatory and anti-inflammatory gene expression as well as JNK phosphorylation. Conclusion Gut microbiota induced LPS-dependent macrophage accumulation in WAT, whereas impairment of systemic glucose metabolism was not dependent on LPS. These results indicate that macrophage accumulation in WAT does not always correlate with impaired glucose metabolism.
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1Abridged Index Medicus
2Adipose Tissue, White - immunology
3Adipose Tissue, White - metabolism
4Adipose Tissue, White - pathology
5Animals
6Biological and medical sciences
7Biomarkers - metabolism
8cardiovascular disease
9colonic microflora
10Diabetes. Impaired glucose tolerance
11diet-induced obesity
12E coli
13Endocrine pancreas. Apud cells (diseases)
14Endocrinopathies
15endotoxemia
16Endotoxin
17energy metabolism
18Escherichia
19Escherichia coli - metabolism
20escherichia-coli
21Etiopathogenesis. Screening. Investigations. Target tissue resistance
22Flow Cytometry
23Gastroenterologi
24Gastroenterology and Hepatology
25Gastroenterology. Liver. Pancreas. Abdomen
26Germ-Free Life
27Glucose
28Glucose intolerance
29Glucose Intolerance - immunology
30Glucose Intolerance - metabolism
31Glucose Intolerance - microbiology
32Glucose Intolerance - pathology
33Glucose metabolism
34gnotobiotic mice
35gut microbiota
36Immunoblotting
37Immunohistochemistry
38inflammation
39Inflammation - immunology
40Inflammation - metabolism
41Inflammation - microbiology
42Inflammation - pathology
43inflammatory diseases
44innate immunity
45Insulin Resistance
46intestinal epithelium
47intestinal permeability
48intestinal tract
49Intestines - microbiology
50Laboratories
51lipid metabolism
52lipids (amino acids
53Lipopolysaccharides - metabolism
54lps
55Macrophages
56Macrophages - metabolism
57macrophages, obesity
58Male
59Medical sciences
60Metabolic disorders
61metabolic inflammation
62metabolic inflammation, inflammation
63Mice
64microbiota
65Microbiota (Symbiotic organisms)
66modifications
67mucosal immunity
68Obesity
69Original
70Original Articles
71peptides
72prebiotic
73proteins
74resistance
75Reverse Transcriptase Polymerase Chain Reaction
76Rodents
77tissue
78toll-like receptors
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6Cani, Patrice D
7Bäckhed, Fredrik
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titleGut-derived lipopolysaccharide augments adipose macrophage accumulation but is not essential for impaired glucose or insulin tolerance in mice
authorCaesar, Robert ; Reigstad, Christopher S ; Bäckhed, Helene Kling ; Reinhardt, Christoph ; Ketonen, Maria ; Östergren Lundén, Gunnel ; Cani, Patrice D ; Bäckhed, Fredrik
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01506
1Abridged Index Medicus
2Adipose Tissue, White - immunology
3Adipose Tissue, White - metabolism
4Adipose Tissue, White - pathology
5Animals
6Biological and medical sciences
7Biomarkers - metabolism
8cardiovascular disease
9colonic microflora
10Diabetes. Impaired glucose tolerance
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13Endocrine pancreas. Apud cells (diseases)
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15endotoxemia
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17energy metabolism
18Escherichia
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26Germ-Free Life
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31Glucose Intolerance - microbiology
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34gnotobiotic mice
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64microbiota
65Microbiota (Symbiotic organisms)
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67mucosal immunity
68Obesity
69Original
70Original Articles
71peptides
72prebiotic
73proteins
74resistance
75Reverse Transcriptase Polymerase Chain Reaction
76Rodents
77tissue
78toll-like receptors
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atitleGut-derived lipopolysaccharide augments adipose macrophage accumulation but is not essential for impaired glucose or insulin tolerance in mice
jtitleGut
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abstractBackground Obesity is associated with accumulation of macrophages in white adipose tissue (WAT), which contribute to the development of insulin resistance. Germ-free (GF) mice have reduced adiposity and are protected against diet-induced obesity, Objective To investigate whether the gut microbiota and, specifically, gut-derived lipopolysaccharide (LPS) promote WAT inflammation and contribute to impaired glucose metabolism. Method Macrophage composition and expression of proinflammatory and anti-inflammatory markers were compared in WAT of GF, conventionally raised and Escherichia coli-monocolonised mice. Additionally, glucose and insulin tolerance in these mice was determined. Results The presence of a gut microbiota resulted in impaired glucose metabolism and increased macrophage accumulation and polarisation towards the proinflammatory M1 phenotype in WAT. Monocolonisation of GF mice for 4 weeks with E.coli W3110 or the isogenic strain MLK1067 (which expresses LPS with reduced immunogenicity) resulted in impaired glucose and insulin tolerance and promoted M1 polarisation of CD11b cells in WAT. However, colonisation with E.coli W3110 but not MLK1067 promoted macrophage accumulation and upregulation of proinflammatory and anti-inflammatory gene expression as well as JNK phosphorylation. Conclusion Gut microbiota induced LPS-dependent macrophage accumulation in WAT, whereas impairment of systemic glucose metabolism was not dependent on LPS. These results indicate that macrophage accumulation in WAT does not always correlate with impaired glucose metabolism.
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pmid22535377
doi10.1136/gutjnl-2011-301689
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