Metabolic adaptation to a high-fat diet is associated with a change in the gut microbiota
By M. Serino, E. Luche, S. Grés, Audrey Baylac, M. Bergé, C. Cénac, A. Waget, P. Klopp, J. Iacovoni, C. Klopp and 11 more. Gut, 2011
605 citations recorded by the source corpus.
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.
Subfields: Endocrinology, Diabetes and Metabolism, Epidemiology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/d87c492e234f3be1ac11716c2d3b2da21ec180c1
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In Endocrinology, Diabetes and Metabolism
In Epidemiology
In Molecular Biology
- J. Whooley
- R. D'Incà
- Sara Vieira-Silva
- Jeroen Raes
- Mehrdad Hajibabaei
- R. Ross
- Andrea Michielan
- S. Bischoff
Citations in the corpus
- How informative is the mouse for human gut microbiota research? (2015, background): “microbiota composition and metabolic adaptations in mice on highfat diets (Serino et al., 2012).”
- Intestinal permeability – a new target for disease prevention and therapy (2014, background): “New data suggest that intestinal barrier and intestinal microbiota play a role in many different diseases such as idiopathic liver fibrosis or intestinal dysbiosis the mechanism of which were largely unclear until recently [11-13].”
- Low-grade inflammation, diet composition and health: current research evidence and its translation (2015, neutral): “In a recent dietary intervention study in male C57Bl/6 mice, the alteration in microbiota profiles as a result of a high-fat diet was strongly associated with gut permeability, endotoxaemia and adipose tissue inflammation((24)).”
- Next‐generation sequencing technologies for environmental DNA research (2012, background): “Also, several studies have been conducted on the effect of diet on the gut microbiome of mice using 16S rDNA amplicons (Turnbaugh et al. 2008, 2009; Murphy et al. 2010; Ravussin et al. 2011; Serino et al. 2011).”
- Intestinal Permeability in Inflammatory Bowel Disease: Pathogenesis, Clinical Evaluation, and Therapy of Leaky Gut (2015, background): “Western diet with its high content of fat and refined sugars is a risk factor for the development of CD [109] probably inducing a low-grade inflammation via gut dysbiosis and increased intestinal permeability [110–112].”
- The Gut Microbiota of Marine Fish (2018, positive): “The influence of diet on gut microbiota is a logical link and has been reported numerous times for an array of species (Claesson et al., 2012; Serino et al., 2012; Miyake et al., 2015; Li et al., 2017).”