Article Text
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.
- Gut microbes pyrosequencing
- metabolic heterogeneity
- high-fat diet responsiveness
- type 2 diabetes
- bacterial translocation
- intestinal barrier function
- intestinal bacteria
- bone marrow transplantation
- diabetes mellitus
- gastrointestinal physiology
- diabetes mellitus
- ANAL
- diabetes mellitus
- diabetes mellitus
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Supplementary materials
Supplementary Data
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Files in this Data Supplement:
- Data supplement 1 - Online figure 1
- Data supplement 2 - Online figure 2
- Data supplement 3 - Online figure 3
- Data supplement 4 - Online figure 4
- Data supplement 5 - Online figure 5
- Data supplement 6 - Online figure 6
- Data supplement 7 - Online figure 7
- Data supplement 8 - Online table 1
- Data supplement 9 - Online table 2
Footnotes
See Commentary, p 474
Funding This work was supported by grants from Agence Nationale pour la Recherche (ANR) to RB and collaborators (ANR-Florinflam and Transflora); in part, by the European Commission's Seventh Framework programme under grant agreement No 241913 (FLORINASH) to RB and by the Benjamin Delessert Foundation to MS.
Competing interests None.
Provenance and peer review Not commissioned; externally peer reviewed.
Linked Articles
- Commentary