Brain-gut-microbiome interactions in obesity and food addiction.

Brain-gut-microbiome interactions in obesity and food addiction.
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DOI:
10.1038/s41575-020-0341-5
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发表时间:
2020-11
期刊:
Nature reviews. Gastroenterology & hepatology
影响因子:
--
通讯作者:
Mayer EA
Mayer EA
中科院分区:
其他
文献类型:
--
作者:
Gupta A;Osadchiy V;Mayer EA

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正常的饮食行为是由肠道和肠外的动态平衡和享乐机制之间严格调节的平衡来协调的。相比之下,食物成瘾代表了一种复杂的、不适应的饮食行为,反映了大脑-肠道-微生物组(BGM)相互作用的变化,以及这种平衡向享乐机制的转变。BGM轴的每个组成部分都与食物成瘾的发展有关,大脑到肠道和肠道到大脑的信号都发挥了作用。早期生活的影响可以为婴儿的肠道微生物群和大脑的食物成瘾做好准备,而成年期抗生素使用的增加和饮食模式的增加可能会进一步加强这一点。廉价、高口感和高热量食物的无处不在的可获得性和营销可以通过中枢(多巴胺能信号中断)和肠道(迷走神经传入功能、代谢性毒血症、系统免疫激活、肠道微生物组和代谢组的变化)机制进一步将这种平衡转向享乐饮食。在这篇综述中,我们提出了一个BGM相互作用的系统生物学模型,该模型结合了已发表的关于食物成瘾的报告,并为针对BGM轴的每个水平的治疗靶点提供了新的见解。
Normal eating behavior is coordinated by the tightly regulated balance between intestinal and extra-intestinal homeostatic and hedonic mechanisms. By contrast, food addiction represents a complex, maladaptive eating behavior that reflects alterations in brain–gut–microbiome (BGM) interactions and a shift of this balance towards hedonic mechanisms. Each component of the BGM axis has been implicated in the development of food addiction, with both brain to gut and gut to brain signaling playing a role. Early life influences can prime the infant gut microbiome and brain for food addiction, which might be further reinforced by increased antibiotic usage and dietary patterns throughout adulthood. The ubiquitous availability and marketing of inexpensive, highly palatable and calorie dense food can further shift this balance towards hedonic eating through both central (disruptions in dopaminergic signaling) and intestinal (vagal afferent function, metabolic toxaemia, systemic immune activation, changes to gut microbiome and metabolome) mechanisms. In this Review, we propose a systems biological model of BGM interactions, which incorporates published reports on food addiction, and provides novel insights into treatment targets aimed at each level of the BGM axis.
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