High fat diet drives obesity regardless the composition of gut microbiota in mice

• Published in: Scientific reports Vol. 6; no. 1; p. 32484
• Main Authors: Rabot, Sylvie, Membrez, Mathieu, Blancher, Florence, Berger, Bernard, Moine, Déborah, Krause, Lutz, Bibiloni, Rodrigo, Bruneau, Aurélia, Gérard, Philippe, Siddharth, Jay, Lauber, Christian L., Chou, Chieh Jason
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 31.08.2016; Nature Publishing Group
• Subjects: 38/22; 38/23; 38/77; 38/90; 631/326/2565/2134; 692/699/2743/137; 692/699/2743/393; Abundance; Animal models; Body weight; Body weight gain; Feed conversion; Feed efficiency; Feeding; Glucose; Glucose metabolism; Glucose tolerance; High fat diet; Humanities and Social Sciences; Immunological tolerance; Inoculation; Insulin; Intestinal microflora; Intolerance; Life Sciences; Metabolism; multidisciplinary; Obesity; Phenotypic variations; Rodents; Science; Science (multidisciplinary); Transplantation; glucose; insulin-resistance; weight-gain; cells; inflammation; metabolism; sensitivity; mechanisms; enterotypes
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/srep32484

The gut microbiota is involved in many aspects of host physiology but its role in body weight and glucose metabolism remains unclear. Here we studied the compositional changes of gut microbiota in diet-induced obesity mice that were conventionally raised or received microbiota transplantation. In conventional mice, the diversity of the faecal microbiota was weakly associated with 1 st week weight gain but transferring the microbiota of mice with contrasting weight gain to germfree mice did not change obesity development or feed efficiency of recipients regardless whether the microbiota was taken before or after 10 weeks high fat (HF) feeding. Interestingly, HF-induced glucose intolerance was influenced by microbiota inoculation and improved glucose tolerance was associated with a low Firmicutes to Bacteroidetes ratio. Transplantation of Bacteroidetes rich microbiota compared to a control microbiota ameliorated glucose intolerance caused by HF feeding. Altogether, our results demonstrate that gut microbiota is involved in the regulation of glucose metabolism and the abundance of Bacteroidetes significantly modulates HF-induced glucose intolerance but has limited impact on obesity in mice. Our results suggest that gut microbiota is a part of complex aetiology of insulin resistance syndrome, individual microbiota composition may cause phenotypic variation associated with HF feeding in mice.