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The effect of short-term exposure to energy-matched diets enriched in fat or sugar on memory, gut microbiota and markers of brain inflammation and plasticity

机译:短期暴露于能量匹配的富含脂肪或糖的饮食对记忆,肠道菌群以及脑部炎症和可塑性标志物的影响

摘要

© 2016 Elsevier Inc. Short-term exposure to high-energy diets impairs memory but there is little data on the relative contributions of fat and sugar to these deficits or the mechanisms responsible. Here, we investigated how these different macronutrients affect memory, neuroinflammation and neuroplasticity markers and the gut microbiota. Rats were fed matched purified diets for 2 weeks; Control, Sugar, Saturated Fatty Acid (SFA) or Polyunsaturated Fatty Acid (PUFA), which varied only in the percentage of energy available from sugar and the amount and type of fat. Rats consuming SFA and Sugar were impaired on hippocampal-dependent place recognition memory compared to Controls and PUFA rats, despite all rats consuming similar amounts of energy. All rats performed comparably on the object recognition task. Hippocampal and hypothalamic inflammatory markers were not substantially affected by the diets and there was no change in the neuroplasticity marker, brain-derived neurotrophic factor. Each of the diets significantly altered the microbial composition in distinct ways. Specifically, the relative abundance of 89 taxa differed significantly between groups with the majority of these changes accounted for by the Clostridiales order and within that, Lachnospiraceae and Ruminococcaceae. These taxa showed a range of macronutrient specific correlations with place memory. In addition, Distance based Linear Models found relationships between memory, inflammation-related hippocampal genes and the gut microbiota. In conclusion, our study shows that the macronutrient profile of the diet is crucial for diet-induced memory deficits and suggests a possible link between diet, the gut microbiota and hippocampal inflammatory genes.
机译:©2016 Elsevier Inc.短期暴露于高能量饮食会损害记忆力,但很少有关于脂肪和糖对这些缺陷或相关机制的相对贡献的数据。在这里,我们研究了这些不同的常量营养素如何影响记忆力,神经炎症和神经可塑性标志物以及肠道菌群。给大鼠喂食相匹配的纯化饮食2周;对照,糖,饱和脂肪酸(SFA)或多不饱和脂肪酸(PUFA),其变化仅在于糖的可用能量百分比以及脂肪的数量和类型。与对照组和PUFA大鼠相比,食用SFA和糖的大鼠的海马依赖性位置识别记忆受到损害,尽管所有大鼠均消耗相似量的能量。所有大鼠在对象识别任务上的表现均相当。饮食对海马和下丘脑炎性标志物没有实质性影响,神经可塑性标志物,脑源性神经营养因子也没有变化。每种饮食都以不同的方式显着改变了微生物的组成。具体而言,各组之间89个分类单元的相对丰度有显着差异,其中大多数变化是梭状芽胞杆菌科(其中梭毛藻科和羽球菌科)造成的。这些分类单元显示了一系列与位置记忆相关的大量营养素特异性相关性。此外,基于距离的线性模型还发现了记忆,炎症相关海马基因与肠道菌群之间的关系。总之,我们的研究表明,饮食中的丰富营养素对于饮食引起的记忆缺陷至关重要,并表明饮食,肠道菌群和海马炎症基因之间可能存在联系。

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