Microbiota, intestine, and brain interact one with another through the afferent fibers of the vagus nerve, which is the major linkage of this one. It has been established that long-term dietary habits influence gut bacterial diversity and are capable of inducing changes in hypothalamic energy homeostasis. The biological effects are mediated by microglial activation, systemic inflammation, and vagal afferent nerve signaling, culminating in neuroinflammation. It has been emphasized the need for a further approach regarding the influence of the dietary factors as well as their direct impacts or outcomes on the gut dysbiosis. This review aimed to understand the role of some dietary triggers of neuroinflammation on changes in the gut microbiota. Each of the diets significantly altered the microbial composition in distinct ways, leading to neuroadaptations. Hyperlipidic diets (SFA and MUFA) can stimulate TLR4 inflammatory pathway by increased LPS translocation and LBP activation and modulate brain functions, mainly in the center of feeding. Overconsumption of sucrose seems to be more detrimental for metabolic alterations, whereas fructose has a more pronounced effect on gut barrier dysfunction and subclinical inflammation; nevertheless, sucrose absorption favors fructose bioavailability, contributing to adiposity and sugar addiction.

中文翻译：

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高脂或高糖饮食会触发微生物菌群-肠脑轴的炎症。

微生物群，肠子和大脑通过迷走神经的传入纤维彼此相互作用，这是该迷走神经的主要联系。已经确定长期的饮食习惯会影响肠道细菌的多样性，并能够引起下丘脑能量稳态的变化。生物学作用是由小胶质细胞活化，全身性炎症和迷走神经传入神经信号介导的，最终导致神经炎症。人们已经强调，有必要采取进一步措施来解决饮食因素的影响及其对肠道营养不良的直接影响或结果。这篇综述旨在了解饮食中一些神经炎症触发因素对肠道菌群变化的作用。每种饮食都以不同的方式显着改变了微生物的组成，导致神经适应。高脂饮食（SFA和MUFA）可以通过增加LPS易位和LBP活化来刺激TLR4炎症途径，并主要在喂养中心调节脑功能。过量摄入蔗糖似乎对代谢改变更有害，而果糖对肠屏障功能障碍和亚临床炎症有更明显的影响。但是，蔗糖的吸收有利于果糖的生物利用度，有助于肥胖和糖瘾。果糖对肠屏障功能障碍和亚临床炎症有更明显的影响；但是，蔗糖的吸收有利于果糖的生物利用度，有助于肥胖和糖瘾。果糖对肠屏障功能障碍和亚临床炎症有更明显的影响；但是，蔗糖的吸收有利于果糖的生物利用度，有助于肥胖和糖瘾。