ena-STUDY-UNIVERSITY OF NORTH CAROLINA AT CHAPEL HILL-28-02-2017-19:38:59:819-20
High fat diet (HFD) induces elevated inflammation in the Nlrp12–/– mice, which leads to an increased obesity and gut dysbiosis. Transferring the microbiota from the WT mice by cohousing attenuates the obesity signs and increases the relative abundance of Clostridiales and Lachnospiraceae. Transferring the isolated Lachnospiraceae also attenuated the obesity and inflammation
HFD can induced obesity-related inflammation, which we found induced commensal bacterial dysbiosis.  We have identified that Nlrp12–/– mice are more susceptible to  HFD-induced dysbiosis and obesity. And these dysbiosis were observed in both vivaria at University of North Carolina at Chapel Hill.   While, cohousing Nlrp12–/– mice with WT mice leads to an increased Clostridiales and Lachnospiraceae in the Nlrp12–/– mice, which attenuated the obesity. We isolated the Lachnospiraceae bacterial groups from the WT mice and transferred them into the HFD-fed Nlrp12–/– mice, which also attenuated the weight gain and the dysbiosis in the Nlrp12–/– mice.
HFD can induced obesity-related inflammation, which we found induced commensal bacterial dysbiosis.  We have identified that Nlrp12–/– mice are more susceptible to  HFD-induced dysbiosis and obesity. And these dysbiosis were observed in both vivaria at University of North Carolina at Chapel Hill.   While, cohousing Nlrp12–/– mice with WT mice leads to an increased Clostridiales and Lachnospiraceae in the Nlrp12–/– mice, which attenuated the obesity. We isolated the Lachnospiraceae bacterial groups from the WT mice and transferred them into the HFD-fed Nlrp12–/– mice, which also attenuated the weight gain and the dysbiosis in the Nlrp12–/– mice.