The gut microbiota modulate locomotion via vagus-dependent glucagon-like peptide-1 signaling

Tzu Ting Lai, Yu Hsuan Tsai, Chia Wei Liou, Ching Hsiang Fan, Yu Tian Hou, Tzu Hsuan Yao, Hsiao Li Chuang, Wei Li Wu

研究成果: Article同行評審

5 引文 斯高帕斯(Scopus)

摘要

Locomotor activity is an innate behavior that can be triggered by gut-motivated conditions, such as appetite and metabolic condition. Various nutrient-sensing receptors distributed in the vagal terminal in the gut are crucial for signal transduction from the gut to the brain. The levels of gut hormones are closely associated with the colonization status of the gut microbiota, suggesting a complicated interaction among gut bacteria, gut hormones, and the brain. However, the detailed mechanism underlying gut microbiota-mediated endocrine signaling in the modulation of locomotion is still unclear. Herein, we show that broad-spectrum antibiotic cocktail (ABX)-treated mice displayed hypolocomotion and elevated levels of the gut hormone glucagon-like peptide-1 (GLP-1). Blockade of the GLP-1 receptor and subdiaphragmatic vagal transmission rescued the deficient locomotor phenotype in ABX-treated mice. Activation of the GLP-1 receptor and vagal projecting brain regions led to hypolocomotion. Finally, selective antibiotic treatment dramatically increased serum GLP-1 levels and decreased locomotion. Colonizing Lactobacillus reuteri and Bacteroides thetaiotaomicron in microbiota-deficient mice suppressed GLP-1 levels and restored the hypolocomotor phenotype. Our findings identify a mechanism by which specific gut microbes mediate host motor behavior via the enteroendocrine and vagal-dependent neural pathways.

原文English
文章編號2
期刊npj Biofilms and Microbiomes
10
發行號1
DOIs
出版狀態Published - 2024 12月

All Science Journal Classification (ASJC) codes

  • 生物技術
  • 微生物學
  • 應用微生物與生物技術

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