Differential colonization with segmented filamentous bacteria and Lactobacillus murinus do not drive divergent development of diet-induced obesity in C57BL/6 mice.
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.
Division of Cellular and Molecular Immunology, Cincinnati Children's Hospital Research Foundation, Cincinnati 45229, OH, USA ; The University of Cincinnati College of Medicine, Cincinnati 45229, OH, USA.
Isaac T W
IT
Harley
Daniel A
DA
Giles
Paul T
PT
Pfluger
Stacey L
SL
Burgess
Stephanie
S
Walters
Jazzminn
J
Hembree
Christine
C
Raver
Cheryl L
CL
Rewerts
Jordan
J
Downey
Leah M
LM
Flick
Traci E
TE
Stankiewicz
Jaclyn W
JW
McAlees
Marsha
M
Wills-Karp
R
R
Balfour Sartor
Senad
S
Divanovic
Matthias H
MH
Tschöp
Christopher L
CL
Karp
Inflammation; Metabolism; Microbiome; Nicotinamide nucleotide transhydrogenase; Obesity