Differential colonization with segmented filamentous bacteria and Lactobacillus murinus do not drive divergent development of diet-induced obesity in C57BL/6 mice.

Abstract

Alterations in the gut microbiota have been proposed to modify the development and maintenance of obesity and its sequelae. Definition of underlying mechanisms has lagged, although the ability of commensal gut microbes to drive pathways involved in inflammation and metabolism has generated compelling, testable hypotheses. We studied C57BL/6 mice from two vendors that differ in their obesogenic response and in their colonization by specific members of the gut microbiota having well-described roles in regulating gut immune responses. We confirmed the presence of robust differences in weight gain in mice from these different vendors during high fat diet stress. However, neither specific, highly divergent members of the gut microbiota (Lactobacillus murinus, segmented filamentous bacteria) nor the horizontally transmissible gut microbiota were found to be responsible. Constitutive differences in locomotor activity were observed, however. These data underscore the importance of selecting appropriate controls in this widely used model of human obesity.

DOI: 10.1016/j.molmet.2013.04.004

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@article{Harley2013DifferentialCW, title={Differential colonization with segmented filamentous bacteria and Lactobacillus murinus do not drive divergent development of diet-induced obesity in C57BL/6 mice.}, author={Isaac T. W. Harley and Daniel Aaron Giles and Paul T Pfluger and Stacey L. Burgess and Stephanie Walters and Jazzminn L. Hembree and Christine Raver and Cheryl L. Rewerts and Jordan Downey and Leah M. Flick and Traci E. Stankiewicz and Jaclyn W. McAlees and Marsha Wills-Karp and R. Balfour Sartor and Senad Divanovic and Matthias H Tsch{\"{o}p and Christopher L . Karp}, journal={Molecular metabolism}, year={2013}, volume={2 3}, pages={171-83} }