Journal
CELL REPORTS
Volume 18, Issue 7, Pages 1739-1750Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2017.01.062
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Funding
- NIH [DK108259, DK101573, DK102948, R24DK091207, RR021940, GM077336]
- Clinical and Translational Science Award (CTSA) program, through the NIH National Center for Advancing Translational Sciences (NCATS) [UL1TR000427, KL2TR000428]
- National Center for Advancing Translational Science [UL1TR000427, KL2TR000428]
- NLM Computation and Informatics in Biology and Medicine Postdoctoral Fellowship [5T15LM007359]
- NIH National Institute of Allergy and Infectious Diseases [T32AI55397]
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Genetic variation drives phenotypic diversity and influences the predisposition to metabolic disease. Here, we characterize the metabolic phenotypes of eight genetically distinct inbred mouse strains in response to a high-fat/high- sucrose diet. We found significant variation in diabetes-related phenotypes and gut microbiota composition among the different mouse strains in response to the dietary challenge and identified taxa associated with these traits. Follow-up microbiota transplant experiments showed that altering the composition of the gut microbiota modifies strain-specific susceptibility to diet-induced metabolic disease. Animals harboring microbial communities with enhanced capacity for processing dietary sugars and for generating hydrophobic bile acids showed increased susceptibility to metabolic disease. Notably, differences in glucosestimulated insulin secretion between different mouse strains were partially recapitulated via gut microbiota transfer. Our results suggest that the gut microbiome contributes to the genetic and phenotypic diversity observed among mouse strains and provide a link between the gut microbiome and insulin secretion.
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