肥胖肠道菌群如何促进焦虑和抑郁?
  • 高脂饮食诱导的肥胖(DIO)小鼠,焦虑和抑郁样行为增多;
  • DIO小鼠口服甲硝唑或万古霉素,可降低伏隔核等大脑区域的炎性细胞因子表达,改善大脑和外围的胰岛素抵抗,减少焦虑和抑郁行为;
  • 这些效果可逆,也可通过粪菌移植在无菌小鼠中重现;
  • 代谢组分析表明,抗生素可使DIO小鼠脑内的色氨酸、GABA、脑源性神经营养因子、氨基酸和多种酰基肉毒碱的水平正常化;
  • 肠道菌群的变化,控制大脑的胰岛素信号和代谢物水平,影响神经行为。
主编推荐语
mildbreeze
糖尿病和肥胖可能增加焦虑和抑郁行为,Molecular Psychiatry本周的一项动物研究,阐释了肠道菌群在其中的关键作用。该研究表明高脂饮食诱导的肥胖,可改变脑内胰岛素敏感度和神经递质等代谢物水平,引起焦虑和抑郁,而口服抗生素可以逆转。这些结果有助于加深对肠脑轴以及肠道菌群调节宿主行为的机制的理解,并为相关干预手段带来启示。
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Gut microbiota modulate neurobehavior through changes in brain insulin sensitivity and metabolism

通过大脑中胰岛素敏感度和代谢的变化,肠道菌群调节神经行为

10.1038/s41380-018-0086-5

2018-06-18, Article

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Obesity and diabetes in humans are associated with increased rates of anxiety and depression. To understand the role of the gut microbiome and brain insulin resistance in these disorders, we evaluated behaviors and insulin action in brain of mice with diet-induced obesity (DIO) with and without antibiotic treatment. We find that DIO mice have behaviors reflective of increased anxiety and depression. This is associated with decreased insulin signaling and increased inflammation in in the nucleus accumbens and amygdala. Treatment with oral metronidazole or vancomycin decreases inflammation, improves insulin signaling in the brain and reduces signs of anxiety and depression. These effects are associated with changes in the levels of tryptophan, GABA, BDNF, amino acids, and multiple acylcarnitines, and are transferable to germ-free mice by fecal transplant. Thus, changes in gut microbiota can control brain insulin signaling and metabolite levels, and this leads to altered neurobehaviors.

First Authors:
Marion Soto

Correspondence Authors:
C Ronald Kahn

All Authors:
Marion Soto,Clémence Herzog,Julian A Pacheco,Shiho Fujisaka,Kevin Bullock,Clary B Clish,C Ronald Kahn

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