title: Metabolic adaptation to a high-fat diet is associated with a change in the gut microbiota.
abstract: 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.
authors: Institut National de la Santé et de la Recherche Médicale, Toulouse, France.
authors: Matteo
authors: M
authors: Serino
authors: Elodie
authors: E
authors: Luche
authors: Sandra
authors: S
authors: Gres
authors: Audrey
authors: A
authors: Baylac
authors: Mathieu
authors: M
authors: Bergé
authors: Claire
authors: C
authors: Cenac
authors: Aurelie
authors: A
authors: Waget
authors: Pascale
authors: P
authors: Klopp
authors: Jason
authors: J
authors: Iacovoni
authors: Christophe
authors: C
authors: Klopp
authors: Jerome
authors: J
authors: Mariette
authors: Olivier
authors: O
authors: Bouchez
authors: Jerome
authors: J
authors: Lluch
authors: Francoise
authors: F
authors: Ouarné
authors: Pierre
authors: P
authors: Monsan
authors: Philippe
authors: P
authors: Valet
authors: Christine
authors: C
authors: Roques
authors: Jacques
authors: J
authors: Amar
authors: Anne
authors: A
authors: Bouloumié
authors: Vassilia
authors: V
authors: Théodorou
authors: Remy
authors: R
authors: Burcelin
mesh_terms: D000222:Adaptation, Physiological / Q000502:physiology*; D000818:Animals; D002432:Cecum / Q000382:microbiology; D016207:Cytokines / Q000097:blood; D003921:Diabetes Mellitus, Experimental / Q000097:blood / Q000503:physiopathology; D059305:Diet, High-Fat; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005951:Glucose Tolerance Test; D007408:Intestinal Absorption / Q000502:physiology; D007422:Intestines / Q000382:microbiology*; D008070:Lipopolysaccharides / Q000097:blood; D008099:Liver / Q000378:metabolism; D008297:Male; D054892:Metagenome / Q000502:physiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D018482:Muscle, Skeletal / Q000378:metabolism; D010539:Permeability; D010641:Phenotype
chemical_list: D016207:Cytokines; D005230:Fatty Acids, Nonesterified; D008070:Lipopolysaccharides