Journal
CELL METABOLISM
Volume 17, Issue 1, Pages 141-152Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2012.12.007
Keywords
-
Categories
Funding
- National Institutes of Health (NIH) [HL028481, HL30568, DK094311]
- Howard Hughes Medical Institute Early Career Scientist award
- NIH [T32-HD07228, T32-HL69766, T32-GM08759]
- MOBILITAS Postdoctoral Research Grant [MJD252]
- American Heart Association postdoctoral fellowship [10POST3660048]
- Div Of Information & Intelligent Systems
- Direct For Computer & Info Scie & Enginr [0916676] Funding Source: National Science Foundation
Ask authors/readers for more resources
Obesity is a highly heritable disease driven by complex interactions between genetic and environmental factors. Human genome-wide association studies (GWAS) have identified a number of loci contributing to obesity; however, a major limitation of these studies is the inability to assess environmental interactions common to obesity. Using a systems genetics approach, we measured obesity traits, global gene expression, and gut microbiota composition in response to a high-fat/high-sucrose (HF/HS) diet of more than 100 inbred strains of mice. Here we show that HF/HS feeding promotes robust, strain-specific changes in obesity that are not accounted for by food intake and provide evidence for a genetically determined set point for obesity. GWAS analysis identified 11 genome-wide significant loci associated with obesity traits, several of which overlap with loci identified in human studies. We also show strong relationships between genotype and gut microbiota plasticity during HF/HS feeding and identify gut microbial phylotypes associated with obesity.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available