Increased evidences demonstrated that gut microbiota targeted diet intervention can alleviate obesity and related metabolic disorders. The underlying mechanism of interactions among diet, microbiota and host still remains unclear. Enterobacter cloacae B29, an endotoxin-producing strain dominated in the gut of a morbidly obese volunteer (weight 174.8 kg, BMI 58.8 kg m-2) was isolated and transplanted to germfree mice. Using deep mRNA sequencing technology, we compared different gene expression profiles in the colon samples of the germfree mice before and after treated with B29 and/or high fat diet (HFD) and identified 279 differential expressed genes in total, including up-regulated genes Apoa4, Ido1, Cyp4a10, and down-regulated genes Cyp2e1, Cyp26b1, Akr1b7, Adipoq, Cyp1a1, Apoa1, Npc1l1, Tff2, Apoc1, Ctla2a, Mttp, Lpl. Fifty-nine GO biological processes and five KEGG pathways, particularly the Peroxisome proliferator-activated receptors (PPARs) signaling pathway, were significantly enriched in response to HFD+B29, which were mainly relevant to inflammation and the metabolism of lipid, lipoprotein and sterols. These functional changes were consistent with the developed obesity, insulin-resistance, and aggravated inflammatory conditions of the HFD+B29 mice. This work provides insight into the gene expression changes in response to HFD+B29, helping to understand the mechanism of the interactions among HFD, B29 and the germfree mice.
Overall design: Four groups(n=6) of germfree mice treated with: NCD+LB, NCD+B29, HFD+LB, HFD+B29
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