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; Gerald I. Shulman

doi:10.1038/nature18309

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, Gerald I. Shulman

532 Citationer (Scopus)

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.

Originalsprog	Engelsk
Tidsskrift	Nature
Vol/bind	534
Udgave nummer	7606
Sider (fra-til)	213-7
Antal sider	5
ISSN	0028-0836
DOI	https://doi.org/10.1038/nature18309
Status	Udgivet - 8 jun. 2016

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10.1038/nature18309

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title = "Acetate mediates a microbiome-brain-β-cell axis to promote metabolic syndrome",

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.",

keywords = "Acetates, Animals, Brain, Diet, High-Fat, Gastrointestinal Microbiome, Ghrelin, Glucose, Hyperphagia, Insulin, Insulin-Secreting Cells, Metabolic Syndrome X, Obesity, Parasympathetic Nervous System, Rats, Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't",

author = "Perry, {Rachel J} and Liang Peng and Barry, {Natasha A} and Cline, {Gary W} and Dongyan Zhang and Cardone, {Rebecca L} and Petersen, {Kitt Falk} and Kibbey, {Richard G} and Goodman, {Andrew L} and Shulman, {Gerald I.}",

year = "2016",

month = jun,

day = "8",

doi = "10.1038/nature18309",

language = "English",

volume = "534",

pages = "213--7",

journal = "Nature",

issn = "0028-0836",

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TY - JOUR

T1 - Acetate mediates a microbiome-brain-β-cell axis to promote metabolic syndrome

AU - Perry, Rachel J

AU - Peng, Liang

AU - Barry, Natasha A

AU - Cline, Gary W

AU - Zhang, Dongyan

AU - Cardone, Rebecca L

AU - Petersen, Kitt Falk

AU - Kibbey, Richard G

AU - Goodman, Andrew L

AU - Shulman, Gerald I.

PY - 2016/6/8

Y1 - 2016/6/8

N2 - 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.

AB - 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.

KW - Acetates

KW - Animals

KW - Brain

KW - Diet, High-Fat

KW - Gastrointestinal Microbiome

KW - Ghrelin

KW - Glucose

KW - Hyperphagia

KW - Insulin

KW - Insulin-Secreting Cells

KW - Metabolic Syndrome X

KW - Obesity

KW - Parasympathetic Nervous System

KW - Rats

KW - Journal Article

KW - Research Support, N.I.H., Extramural

KW - Research Support, Non-U.S. Gov't

U2 - 10.1038/nature18309

DO - 10.1038/nature18309

M3 - Journal article

C2 - 27279214

SN - 0028-0836

VL - 534

SP - 213

EP - 217

JO - Nature

JF - Nature

IS - 7606

ER -

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

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