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Nature. 2016 Jun 9;534(7606):213-7. doi: 10.1038/nature18309.

Acetate mediates a microbiome-brain-β-cell axis to promote metabolic syndrome.

Author information

1
Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
2
Department of Microbial Pathogenesis, Yale University School of Medicine, New Haven, Connecticut 06510, USA.
3
Microbial Sciences Institute, Yale University School of Medicine, New Haven, Connecticut 06516, USA.
4
Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut 06519, USA.
5
Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, Copenhagen 2200, Denmark.
6
Department of Cellular &Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut 06510, USA.

Abstract

Obesity, insulin resistance and the metabolic syndrome are associated with changes to the gut microbiota; however, the mechanism by which modifications to the gut microbiota might lead to these conditions is unknown. Here we show that increased production of acetate by an altered gut microbiota in rodents leads to activation of the parasympathetic nervous system, which, in turn, promotes increased glucose-stimulated insulin secretion, increased ghrelin secretion, hyperphagia, obesity and related sequelae. Together, these findings identify increased acetate production resulting from a nutrient-gut microbiota interaction and subsequent parasympathetic activation as possible therapeutic targets for obesity.

PMID:
27279214
PMCID:
PMC4922538
DOI:
10.1038/nature18309
[Indexed for MEDLINE]
Free PMC Article

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