Journal
SCIENTIFIC REPORTS
Volume 9, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41598-018-37177-3
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Funding
- NIH [AG041765, AG050135, AG051974, AG056771]
- Diabetes Research Center at Washington University [2 P30 DK020579]
- New Investigator Program Award from the Wisconsin Partnership Program
- Progeria Research Foundation
- Glenn Foundation Award for Research in the Biological Mechanisms of Aging
- ERP Graduate Training Program
- UW-Madison School of Medicine and Public Health
- UW-Madison Department of Medicine
- American Federation for Aging Research (AFAR)
- UW Institute on Aging [NIA T32 AG000213]
- American Heart Association [17PRE33410983]
- University of Wisconsin Carbone Cancer Center Support Grant [P30 CA014520]
- Clinical and Translational Science Award (CTSA) program, through the NIH National Center for Advancing Translational Sciences (NCATS) [UL1TR002373]
- U.S. Department of Veterans Affairs [I01-BX004031]
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Obesity and type 2 diabetes are increasing in prevalence around the world, and there is a clear need for new and effective strategies to promote metabolic health. A low protein (LP) diet improves metabolic health in both rodents and humans, but the mechanisms that underlie this effect remain unknown. The gut microbiome has recently emerged as a potent regulator of host metabolism and the response to diet. Here, we demonstrate that a LP diet significantly alters the taxonomic composition of the gut microbiome at the phylum level, altering the relative abundance of Actinobacteria, Bacteroidetes, and Firmicutes. Transcriptional profiling suggested that any impact of the microbiome on liver metabolism was likely independent of the microbiome-farnesoid X receptor (FXR) axis. We therefore tested the ability of a LP diet to improve metabolic health following antibiotic ablation of the gut microbiota. We found that a LP diet promotes leanness, increases energy expenditure, and improves glycemic control equally well in mice treated with antibiotics as in untreated control animals. Our results demonstrate that the beneficial effects of a LP diet on glucose homeostasis, energy balance, and body composition are unlikely to be mediated by diet-induced changes in the taxonomic composition of the gut microbiome.
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