期刊
CELL METABOLISM
卷 22, 期 4, 页码 658-668出版社
CELL PRESS
DOI: 10.1016/j.cmet.2015.07.026
关键词
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资金
- Swedish Research Council
- Swedish Foundation for Strategic Research
- Swedish Diabetes Foundation
- Swedish Heart Lung Foundation
- Torsten Soderbergs Foundation
- Ragnar Soderbergs Foundation
- Novo Nordisk Foundation
- Knut and Alice Wallenberg Foundation
- TORNADO [FP7-KBBE-222720]
- EU [FP7-KBBE-222639]
- LUA-ALF grant from Vastra Gotalandsregionen
- European Research Council (ERC) Consolidator grant [615362 - METABASE]
- FRFS-WELBIO [WELBIO-CR-2012S-02R]
- ERC [336452-ENIGMO]
- Novo Nordisk Fonden [NNF13OC0008163] Funding Source: researchfish
Dietary lipids may influence the abundance of circulating inflammatory microbial factors. Hence, inflammation in white adipose tissue (WAT) induced by dietary lipids may be partly dependent on their interaction with the gut microbiota. Here, we show that mice fed lard for 11 weeks have increased Toll-like receptor (TLR) activation and WAT inflammation and reduced insulin sensitivity compared with mice fed fish oil and that phenotypic differences between the dietary groups can be partly attributed to differences in microbiota composition. Trif(-/-) and Myd88(-/-) mice are protected against lard-induced WAT inflammation and impaired insulin sensitivity. Experiments in germ-free mice show that an interaction between gut microbiota and saturated lipids promotes WAT inflammation independent of adiposity. Finally, we demonstrate that the chemokine CCL2 contributes to microbiota-induced WAT inflammation in lard-fed mice. These results indicate that gut microbiota exacerbates metabolic inflammation through TLR signaling upon challenge with a diet rich in saturated lipids.
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