Altered intestinal microbiota in mice consuming high-fat diets influence cognitive function

Author:

Ma Weiwei1,Hua Yinan2,Zhou Cui2,Fan Rong3,Benazzouz Sara4,Shen Jiingyi2,Xiao Rong2

Affiliation:

1. Capital Medical University

2. School of Public Health, Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing 100069, China.

3. School of Public Health, Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing 100069, China

4. Laboratory of cellular and molecular biology, faculty of biological sciences, University of Science and Technology Houari Boumediene, Bab Ezzouar, 16111, Algeria.

Abstract

Abstract This study was aiming to verify critical role of gut microbiota linking diet-induced obesity and cognitive dysfunction. After antibiotic treatment, male C57BL/6 mice were subjected to fecal microbiota transplantation (FMT) using fecal microbiota isolated from donor mice fed on various high-fat diets and control basic diet. Novel object recognition test, 16S rRNA gene sequencing of feces and haematoxylineosin staining of hippocampal CA1 area were performed for all mice. The results showed that donor obese mice induced by diets high in long-chain saturated fatty acid (LCSFA), n-6 polyunsaturated fatty acid (n-6 PUFA) and trans fatty acid (TFA) had significant cognitive impairment (all Ps < 0.05) compared with that in control and n-3 polyunsaturated fatty acid (n-3 PUFA) groups. In recipient mice, the similar effect of above high-fat diets was revealed after FMT, while in absence of obesity. The donor mice in LCSFA, medium-chain saturated fatty acid (MCSFA), n-6 PUFA, and TFA groups showed more structural breakage and less nerve cells in hippocampal CA1 area than that in other groups, which was similar to corresponding recipients. According to these results it was concluded that high LCSFA, n-6 PUFA, and TFA diets may impair the cognitive function by damaging the structures of CA1 region in hippocampal through influencing intestinal microbiota in mice.

Publisher

Research Square Platform LLC

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