Acetate mediates a microbiome–brain–β-cell axis to promote metabolic syndrome
Rachel J. Perry,
Liang Peng,
Natasha A. Barry,
Gary W. Cline,
Dongyan Zhang,
Rebecca L. Cardone,
Kitt Falk Petersen,
Richard G. Kibbey,
Andrew L. Goodman and
Gerald I. Shulman ()
Additional contact information
Rachel J. Perry: Yale University School of Medicine
Liang Peng: Yale University School of Medicine
Natasha A. Barry: Yale University School of Medicine
Gary W. Cline: Yale University School of Medicine
Dongyan Zhang: Howard Hughes Medical Institute, Yale University School of Medicine
Rebecca L. Cardone: Yale University School of Medicine
Kitt Falk Petersen: Yale University School of Medicine
Richard G. Kibbey: Yale University School of Medicine
Andrew L. Goodman: Yale University School of Medicine
Gerald I. Shulman: Yale University School of Medicine
Nature, 2016, vol. 534, issue 7606, 213-217
Abstract:
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.
Date: 2016
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Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:534:y:2016:i:7606:d:10.1038_nature18309
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DOI: 10.1038/nature18309
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