Responses of Gut Microbiota and Glucose and Lipid Metabolism to Prebiotics in Genetic Obese and Diet-Induced Leptin-Resistant Mice

By A. Everard, V. Lazarevic, M. Derrien, M. Girard, G. Muccioli, A. Neyrinck, S. Possemiers, Ann Van Holle, Patrice François, W. D. de Vos and 3 more. Diabetes, 2011

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OBJECTIVE To investigate deep and comprehensive analysis of gut microbial communities and biological parameters after prebiotic administration in obese and diabetic mice. RESEARCH DESIGN AND METHODS Genetic (ob/ob) or diet-induced obese and diabetic mice were chronically fed with prebiotic-enriched diet or with a control diet. Extensive gut microbiota analyses, including quantitative PCR, pyrosequencing of the 16S rRNA, and phylogenetic microarrays, were performed in ob/ob mice. The impact of gut microbiota modulation on leptin sensitivity was investigated in diet-induced leptin-resistant mice. Metabolic parameters, gene expression, glucose homeostasis, and enteroendocrine-related L-cell function were documented in both models. RESULTS In ob/ob mice, prebiotic feeding decreased Firmicutes and increased Bacteroidetes phyla, but also changed 102 distinct taxa, 16 of which displayed a >10-fold change in abundance. In addition, prebiotics improved glucose tolerance, increased L-cell number and associated parameters (intestinal proglucagon mRNA expression and plasma glucagon-like peptide-1 levels), and reduced fat-mass development, oxidative stress, and low-grade inflammation. In high fat–fed mice, prebiotic treatment improved leptin sensitivity as well as metabolic parameters. CONCLUSIONS We conclude that specific gut microbiota modulation improves glucose homeostasis, leptin sensitivity, and target enteroendocrine cell activity in obese and diabetic mice. By profiling the gut microbiota, we identified a catalog of putative bacterial targets that may affect host metabolism in obesity and diabetes.

Subfields: Epidemiology, Food Science, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/1cf46d4592eb98cc1b273648fa1fc2f70ab83b98

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Citations in the corpus

Bifidobacteria or fiber protect against diet-induced microbiota-mediated colonic mucus deterioration (2017, background): “Importantly, prebiotic treatment with fiber does not only alter the abundance of Bifidobacterium, but more than 100 other bacterial taxa (Everard et al., 2011).”
Human Gut Microbiota Changes Reveal the Progression of Glucose Intolerance (2013, background): “weight, fat mass and metabolic disorders associated with obesity has been observed [26–29].”
Dietary Polyphenols Promote Growth of the Gut Bacterium Akkermansia muciniphila and Attenuate High-Fat Diet–Induced Metabolic Syndrome (2015, neutral): “muciniphila abundance and similar metabolic improvements (44).”
Cross-talk between Akkermansia muciniphila and intestinal epithelium controls diet-induced obesity (2013, methodology): “Here we investigated the strain that is affected during obesity and type 2 diabetes in humans and rodents (18, 23).”
Human gut microbiome: hopes, threats and promises (2018, background): “82 85 91–93 Importantly, in humans, the abundance of A. muciniphila was seen to be decreased in several pathological conditions, such as obesity, type 2 diabetes, hypertension, hyper-cholesterolaemia and liver disease 94–100 (figure 3).”
Personalized Nutrition by Prediction of Glycemic Responses. (2015, background): “Low levels of Anaerostipes associate with improved glucose tolerance and reduced plasma triglyceride levels in mice (Everard et al., 2011) and indeed these bacteria decrease following the ‘‘good’’ diet and increase following the ‘‘bad’’ diet (Figure 6C).”
Mechanisms and consequences of intestinal dysbiosis (2017, background): “An intake of the prebiotic oligofructose shifts the composition of the gut microbiota towards a lean pattern by increasing Bacteroidetes and reducing Firmicutes in ob/ob mice and in rats genetically prone to develop obesity and insulin resistance [70, 71].”
Microbes inside—from diversity to function: the case of Akkermansia (2012, background): “Genetic-obese mice with diet-induced leptin resistance showed an 80-fold increase in A. muciniphila levels after prebiotic, Fructooligosaccharides, administration, accompanied with increased colon length, size and enteroendocrine L cells (Everard et al., 2011).”
The Western Diet–Microbiome-Host Interaction and Its Role in Metabolic Disease (2018, positive): “When mice were fed a diet that induced metabolic endotoxemia, adding a prebiotic improved metabolic markers [69].”