| Literature DB >> 26638070 |
Claire Chevalier1, Ozren Stojanović1, Didier J Colin2, Nicolas Suarez-Zamorano1, Valentina Tarallo1, Christelle Veyrat-Durebex1, Dorothée Rigo1, Salvatore Fabbiano1, Ana Stevanović1, Stefanie Hagemann3, Xavier Montet4, Yann Seimbille2, Nicola Zamboni5, Siegfried Hapfelmeier3, Mirko Trajkovski6.
Abstract
Microbial functions in the host physiology are a result of the microbiota-host co-evolution. We show that cold exposure leads to marked shift of the microbiota composition, referred to as cold microbiota. Transplantation of the cold microbiota to germ-free mice is sufficient to increase insulin sensitivity of the host and enable tolerance to cold partly by promoting the white fat browning, leading to increased energy expenditure and fat loss. During prolonged cold, however, the body weight loss is attenuated, caused by adaptive mechanisms maximizing caloric uptake and increasing intestinal, villi, and microvilli lengths. This increased absorptive surface is transferable with the cold microbiota, leading to altered intestinal gene expression promoting tissue remodeling and suppression of apoptosis-the effect diminished by co-transplanting the most cold-downregulated strain Akkermansia muciniphila during the cold microbiota transfer. Our results demonstrate the microbiota as a key factor orchestrating the overall energy homeostasis during increased demand.Entities:
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Year: 2015 PMID: 26638070 DOI: 10.1016/j.cell.2015.11.004
Source DB: PubMed Journal: Cell ISSN: 0092-8674 Impact factor: 41.582