Journal
CELL
Volume 181, Issue 6, Pages 1263-+Publisher
CELL PRESS
DOI: 10.1016/j.cell.2020.04.027
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Funding
- Nutrition Science Initiative
- NIH [R01HL122593, R21CA227232, P30DK098722]
- UCSF SSEW Initiative
- Searle Scholars Program [SSP-2016-1352]
- A*STAR
- Pennsylvania Department of Health using Tobacco CURE funds
- Burroughs Wellcome Fund
- Damon Runyon Cancer Research Foundation [DRR-42-16]
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [ZIADK013037] Funding Source: NIH RePORTER
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Very low-carbohydrate, high-fat ketogenic diets (KDs) induce a pronounced shift in metabolic fuel utilization that elevates circulating ketone bodies; however, the consequences of these compounds for host-microbiome interactions remain unknown. Here, we show that KDs alter the human and mouse gut microbiota in a manner distinct from high-fat diets (HFDs). Metagenomic and metabolomic analyses of stool samples from an 8-week inpatient study revealedmarked shifts in gutmicrobial community structure and function during the KD. Gradient diet experiments in mice confirmed the unique impact of KDs relative to HFDs with a reproducible depletion of bifidobacteria. In vitro and in vivo experiments showed that ketone bodies selectively inhibited bifidobacterial growth. Finally, mono-colonizations and human microbiome transplantations into germ-free mice revealed that the KD-associated gut microbiota reduces the levels of intestinal pro-inflammatory Th17 cells. Together, these results highlight the importance of trans-kingdom chemical dialogs for mediating the host response to dietary interventions.
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