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Metabolic adaptation to a high-fat diet is associated with a change in the gut microbiota
- Source :
- Gut, Gut, BMJ Publishing Group, 2012, 61 (4), pp.543-53. ⟨10.1136/gutjnl-2011-301012⟩, Gut 4 (61), 543-553. (2012), Gut; Vol 61, Gut, 2012, 61 (4), pp.543-53. ⟨10.1136/gutjnl-2011-301012⟩
- Publication Year :
- 2012
- Publisher :
- HAL CCSD, 2012.
-
Abstract
- Chantier qualité GA; International audience; OBJECTIVE: The gut microbiota, which is considered a causal factor in metabolic diseases as shown best in animals, is under the dual influence of the host genome and nutritional environment. This study investigated whether the gut microbiota per se, aside from changes in genetic background and diet, could sign different metabolic phenotypes in mice. METHODS: The unique animal model of metabolic adaptation was used, whereby C57Bl/6 male mice fed a high-fat carbohydrate-free diet (HFD) became either diabetic (HFD diabetic, HFD-D) or resisted diabetes (HFD diabetes-resistant, HFD-DR). Pyrosequencing of the gut microbiota was carried out to profile the gut microbial community of different metabolic phenotypes. Inflammation, gut permeability, features of white adipose tissue, liver and skeletal muscle were studied. Furthermore, to modify the gut microbiota directly, an additional group of mice was given a gluco-oligosaccharide (GOS)-supplemented HFD (HFD+GOS). RESULTS: Despite the mice having the same genetic background and nutritional status, a gut microbial profile specific to each metabolic phenotype was identified. The HFD-D gut microbial profile was associated with increased gut permeability linked to increased endotoxaemia and to a dramatic increase in cell number in the stroma vascular fraction from visceral white adipose tissue. Most of the physiological characteristics of the HFD-fed mice were modulated when gut microbiota was intentionally modified by GOS dietary fibres. CONCLUSIONS: The gut microbiota is a signature of the metabolic phenotypes independent of differences in host genetic background and diet.
- Subjects :
- Lipopolysaccharides
Male
mictobiota
White adipose tissue
[SDV.GEN] Life Sciences [q-bio]/Genetics
Gut flora
Fatty Acids, Nonesterified
Intestinal absorption
Cecum
Mice
0302 clinical medicine
gut
metabolic
background
phenotype
diet
MESH: Diabetes Mellitus, Experimental
MESH: Animals
2. Zero hunger
0303 health sciences
Glucose tolerance test
MESH: Muscle, Skeletal
MESH: Cytokines
MESH: Fatty Acids, Nonesterified
medicine.diagnostic_test
biology
digestive, oral, and skin physiology
Gastroenterology
food and beverages
Phenotype
Adaptation, Physiological
Intestines
medicine.anatomical_structure
High-fat diet
Liver
030220 oncology & carcinogenesis
MESH: Permeability
Cytokines
medicine.symptom
MESH: Intestines
medicine.medical_specialty
MESH: Glucose Tolerance Test
MESH: Intestinal Absorption
Médecine humaine et pathologie
Inflammation
Gut microbiota
Diet, High-Fat
MESH: Phenotype
digestive system
Permeability
Diabetes Mellitus, Experimental
03 medical and health sciences
MESH: Mice, Inbred C57BL
Diabetes mellitus
Internal medicine
medicine
Animals
Muscle, Skeletal
MESH: Mice
030304 developmental biology
[SDV.GEN]Life Sciences [q-bio]/Genetics
Metabolic diseases
MESH: Cecum
Glucose Tolerance Test
MESH: Metagenome
medicine.disease
biology.organism_classification
MESH: Adaptation, Physiological
MESH: Male
Mice, Inbred C57BL
MESH: Diet, High-Fat
Endocrinology
Intestinal Absorption
Immunology
Metagenome
MESH: Lipopolysaccharides
MESH: Liver
Subjects
Details
- Language :
- English
- ISSN :
- 00175749 and 14683288
- Database :
- OpenAIRE
- Journal :
- Gut, Gut, BMJ Publishing Group, 2012, 61 (4), pp.543-53. ⟨10.1136/gutjnl-2011-301012⟩, Gut 4 (61), 543-553. (2012), Gut; Vol 61, Gut, 2012, 61 (4), pp.543-53. ⟨10.1136/gutjnl-2011-301012⟩
- Accession number :
- edsair.doi.dedup.....454b327e18ba9a9823003ab3b09e9c20