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高脂肪饮食改变了中年早期 Sprague Dawley 大鼠的肠道微生物群,但不改变其空间工作记忆。

High fat diet alters gut microbiota but not spatial working memory in early middle-aged Sprague Dawley rats.

机构信息

Neurosciences, Furman University, Greenville, South Carolina, United States of America.

Department of Biology, Furman University, Greenville, South Carolina, United States of America.

出版信息

PLoS One. 2019 May 29;14(5):e0217553. doi: 10.1371/journal.pone.0217553. eCollection 2019.

Abstract

As the global population ages, and rates of dementia rise, understanding lifestyle factors that play a role in the development and acceleration of cognitive decline is vital to creating therapies and recommendations to improve quality of later life. Obesity has been shown to increase risk for dementia. However, the specific mechanisms for obesity-induced cognitive decline remain unclear. One potential contributor to diet-induced cognitive changes is neuroinflammation. Furthermore, a source of diet-induced inflammation to potentially increase neuroinflammation is via gut dysbiosis. We hypothesized that a high fat diet would cause gut microbe dysbiosis, and subsequently: neuroinflammation and cognitive decline. Using 7-month old male Sprague Dawley rats, this study examined whether 8 weeks on a high fat diet could impact performance on the water radial arm maze, gut microbe diversity and abundance, and microgliosis. We found that a high fat diet altered gut microbe populations compared to a low fat, control diet. However, we did not observe any significant differences between dietary groups on maze performance (a measure of spatial working memory) or microgliosis. Our data reveal a significant change to the gut microbiome without subsequent effects to neuroinflammation (as measured by microglia characterization and counts in the cortex, hippocampus, and hypothalamus) or cognitive performance under the parameters of our study. However, future studies that explore duration of the diet, composition of the diet, age of animal model, and strain of animal model, must be explored.

摘要

随着全球人口老龄化和痴呆症发病率的上升,了解在认知能力下降的发展和加速中起作用的生活方式因素对于开发治疗方法和提出改善晚年生活质量的建议至关重要。肥胖已被证明会增加痴呆症的风险。然而,肥胖引起认知能力下降的具体机制尚不清楚。饮食引起认知变化的一个潜在因素是神经炎症。此外,饮食引起炎症的一个潜在来源可能是通过肠道菌群失调来增加神经炎症。我们假设高脂肪饮食会导致肠道微生物失调,进而:神经炎症和认知能力下降。本研究使用 7 个月大的雄性 Sprague Dawley 大鼠,研究了高脂肪饮食是否会影响水迷宫的表现、肠道微生物多样性和丰度以及小胶质细胞增生。我们发现,与低脂肪对照饮食相比,高脂肪饮食改变了肠道微生物群。然而,我们没有观察到饮食组之间在迷宫表现(空间工作记忆的衡量标准)或小胶质细胞增生方面有任何显著差异。我们的数据显示,肠道微生物组发生了显著变化,但没有后续影响到神经炎症(通过小胶质细胞特征和大脑皮层、海马体和下丘脑的小胶质细胞计数来衡量)或认知表现,在我们研究的参数下。然而,必须探索研究饮食持续时间、饮食组成、动物模型年龄和动物模型品种等方面的未来研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f63/6541285/5255f5a0465e/pone.0217553.g001.jpg

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