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

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Acetate mediates a microbiome-brain-β-cell axis to promote metabolic syndrome. / Perry, Rachel J; Peng, Liang; Barry, Natasha A; Cline, Gary W; Zhang, Dongyan; Cardone, Rebecca L; Petersen, Kitt Falk; Kibbey, Richard G; Goodman, Andrew L; Shulman, Gerald I.

In: Nature, Vol. 534, No. 7606, 09.06.2016, p. 213-7.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Perry, RJ, Peng, L, Barry, NA, Cline, GW, Zhang, D, Cardone, RL, Petersen, KF, Kibbey, RG, Goodman, AL & Shulman, GI 2016, 'Acetate mediates a microbiome-brain-β-cell axis to promote metabolic syndrome', Nature, vol. 534, no. 7606, pp. 213-7. https://doi.org/10.1038/nature18309

APA

Perry, R. J., Peng, L., Barry, N. A., Cline, G. W., Zhang, D., Cardone, R. L., Petersen, K. F., Kibbey, R. G., Goodman, A. L., & Shulman, G. I. (2016). Acetate mediates a microbiome-brain-β-cell axis to promote metabolic syndrome. Nature, 534(7606), 213-7. https://doi.org/10.1038/nature18309

Vancouver

Perry RJ, Peng L, Barry NA, Cline GW, Zhang D, Cardone RL et al. Acetate mediates a microbiome-brain-β-cell axis to promote metabolic syndrome. Nature. 2016 Jun 9;534(7606):213-7. https://doi.org/10.1038/nature18309

Author

Perry, Rachel J ; Peng, Liang ; Barry, Natasha A ; Cline, Gary W ; Zhang, Dongyan ; Cardone, Rebecca L ; Petersen, Kitt Falk ; Kibbey, Richard G ; Goodman, Andrew L ; Shulman, Gerald I. / Acetate mediates a microbiome-brain-β-cell axis to promote metabolic syndrome. In: Nature. 2016 ; Vol. 534, No. 7606. pp. 213-7.

Bibtex

@article{e06f24e7f28343518bacb9ab55b371ad,
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 = "9",
doi = "10.1038/nature18309",
language = "English",
volume = "534",
pages = "213--7",
journal = "Nature",
issn = "0028-0836",
publisher = "nature publishing group",
number = "7606",

}

RIS

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 - 2016/6/9

Y1 - 2016/6/9

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

VL - 534

SP - 213

EP - 217

JO - Nature

JF - Nature

SN - 0028-0836

IS - 7606

ER -

ID: 166693158