ena-STUDY-SHANGHAI JIAO TONG UNIVERSITY-01-08-2016-02:53:37:980-568
Differential expression of mRNAs in obese germfree mice induced by Enterobacter cloacae B29 combined with the high fat diet
Increased evidences have 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. In this study, Enterobacter cloacae B29, an endotoxin-producing strain dominated in the gut of a morbidly obese volunteer (weight 174.8 kg, body mass index 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 under the stress with B29 and/or high fat diet (HFD) and identified 279 differential expressed genes (DEGs) in total. Both GO and KEGG analysis indicated that these DEGs were mainly relevant to the metabolism of lipid, lipoprotein and sterols, and inflammation. Though many DEGs appeared under the stress of HFD or B29, their functional influences were relatively dispersive. Significant functional changes occurred in response to HFD+B29. In particular, the Peroxisome proliferator-activated receptors (PPARs) signaling pathway was only enriched when HFD and B29 were combined. These observed changes were consistent with the corresponding phenotypes of the mice during the animal trial that only the HFD+B29 group developed obesity, got insulin-resistant phenotypes and aggravated inflammatory conditions. We then picked the key DEGs involved in lipid and lipoprotein metabolism, inflammation and sterol metabolism under the stress of HFD+B29 and described how they respond to the provided stimuli. This work provides insight into the gene expression changes in response to HFD+B29, helping to understand the interactions among the HFD, B29 and the germfree mice, and the phenotype consequences caused by HFD+B29.
Increased evidences have 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. In this study, Enterobacter cloacae B29, an endotoxin-producing strain dominated in the gut of a morbidly obese volunteer (weight 174.8 kg, body mass index 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 under the stress with B29 and/or high fat diet (HFD) and identified 279 differential expressed genes (DEGs) in total. Both GO and KEGG analysis indicated that these DEGs were mainly relevant to the metabolism of lipid, lipoprotein and sterols, and inflammation. Though many DEGs appeared under the stress of HFD or B29, their functional influences were relatively dispersive. Significant functional changes occurred in response to HFD+B29. In particular, the Peroxisome proliferator-activated receptors (PPARs) signaling pathway was only enriched when HFD and B29 were combined. These observed changes were consistent with the corresponding phenotypes of the mice during the animal trial that only the HFD+B29 group developed obesity, got insulin-resistant phenotypes and aggravated inflammatory conditions. We then picked the key DEGs involved in lipid and lipoprotein metabolism, inflammation and sterol metabolism under the stress of HFD+B29 and described how they respond to the provided stimuli. This work provides insight into the gene expression changes in response to HFD+B29, helping to understand the interactions among the HFD, B29 and the germfree mice, and the phenotype consequences caused by HFD+B29.