Acetate mediates a microbiome-brain-β cell axis promoting metabolic syndrome
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Published Date:Jun 09 2016
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Source:Nature. 534(7606):213-217.
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Language:English
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Personal Authors:
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Keywords:
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Pubmed ID:27279214
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Pubmed Central ID:PMC4922538
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Description: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.
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Funding:T32 DK101019/DK/NIDDK NIH HHS/United States
R01 DK-40936/DK/NIDDK NIH HHS/United States
UL1 TR001863/TR/NCATS NIH HHS/United States
U24 DK-59635/DK/NIDDK NIH HHS/United States
R01 GM-103574/GM/NIGMS NIH HHS/United States
U24 DK059635/DK/NIDDK NIH HHS/United States
DP2 GM105456/GM/NIGMS NIH HHS/United States
P30 DK-45735/DK/NIDDK NIH HHS/United States
R01 DK040936/DK/NIDDK NIH HHS/United States
DP2 GM-105456/DP/NCCDPHP CDC HHS/United States
R01 AG023686/AG/NIA NIH HHS/United States
Howard Hughes Medical Institute/United States
P30 DK045735/DK/NIDDK NIH HHS/United States
R01 DK092606/DK/NIDDK NIH HHS/United States
R01 DK-92606/DK/NIDDK NIH HHS/United States
T32 DK-101019/DK/NIDDK NIH HHS/United States
P30 DK034989/DK/NIDDK NIH HHS/United States
R01 GM103574/GM/NIGMS NIH HHS/United States
K01 DK089121/DK/NIDDK NIH HHS/United States
R01 AG-23686/AG/NIA NIH HHS/United States
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