国内外团队合作:β-葡聚糖通过肠脑轴改善肥胖小鼠认知功能
  • 高脂肪低纤维(HFFD)引起肠道菌群改变(拟杆菌门和微生物多样性减少)与肥胖及认知损伤有关;
  • 长期补充β葡聚糖改善HFFD诱导的认知障碍,增加拟杆菌门,促进肠道粘液分泌和上皮的完整性以及免疫稳态;
  • 长期补充β葡聚糖减少革兰氏阴性细菌易位、降低外周炎症并抑制小胶质细胞的神经炎症和突触吞噬;
  • 短期补充β葡聚糖可明显迅速的引起肠道菌群改变,提示菌群改变与认知障碍的因果关系;
  • 抗生素干预消除了β葡聚糖对HFFD的改善作用。
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澳大利亚伍伦贡大学黄旭枫、徐州医科大学郑葵阳和于英华与团队,近期在Microbiome上发表文章,发现长期补充β葡聚糖可改变肠道菌群组成,缓解肥胖诱导的认知损伤,且肠道菌群的改变发生在认知改善之前,证明了肠道菌群和认知障碍之间的因果关系。
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Microbiome [IF:11.607]

β-glucan attenuates cognitive impairment via the gut-brain axis in diet-induced obese mice

β-葡聚糖通过肠脑轴减轻肥胖小鼠的认知损伤

10.1186/s40168-020-00920-y

2020-10-02, Article

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Background: “Western” style dietary patterns are characterized by a high proportion of highly processed foods rich in fat and low in fiber. This diet pattern is associated with a myriad of metabolic dysfunctions, including neuroinflammation and cognitive impairment. β-glucan, the major soluble fiber in oat and barley grains, is fermented in the lower gastrointestinal tract, potentially impacting the microbial ecosystem and thus may improve elements of cognition and brain function via the gut-brain axis. The present study aimed to evaluate the effect of β-glucan on the microbiota gut-brain axis and cognitive function in an obese mouse model induced by a high-fat and fiber-deficient diet (HFFD).
Results: After long-term supplementation for 15 weeks, β-glucan prevented HFFD-induced cognitive impairment assessed behaviorally by object location, novel object recognition, and nesting building tests. In the hippocampus, β-glucan countered the HFFD-induced microglia activation and its engulfment of synaptic puncta, and upregulation of proinflammatory cytokine (TNF-α, IL-1β, and IL-6) mRNA expression. Also, in the hippocampus, β-glucan significantly promoted PTP1B-IRS-pAKT-pGSK3β-pTau signaling for synaptogenesis, improved the synaptic ultrastructure examined by transmission electron microscopy, and increased both pre- and postsynaptic protein levels compared to the HFFD-treated group. In the colon, β-glucan reversed HFFD-induced gut barrier dysfunction increased the thickness of colonic mucus (Alcian blue and mucin-2 glycoprotein immunofluorescence staining), increased the levels of tight junction proteins occludin and zonula occludens-1, and attenuated bacterial endotoxin translocation. The HFFD resulted in microbiota alteration, effects abrogated by long-term β-glucan supplementation, with the β-glucan effects on Bacteroidetes and its lower taxa particularly striking. Importantly, the study of short-term β-glucan supplementation for 7 days demonstrated pronounced, rapid differentiating microbiota changes before the cognitive improvement, suggesting the possible causality of gut microbiota profile on cognition. In support, broad-spectrum antibiotic intervention abrogated β-glucan’s effects on improving cognition, highlighting the role of gut microbiota to mediate cognitive behavior.
Conclusion: This study provides the first evidence that β-glucan improves indices of cognition and brain function with major beneficial effects all along the gut microbiota-brain axis. Our data suggest that elevating consumption of β-glucan-rich foods is an easily implementable nutritional strategy to alleviate detrimental features of gut-brain dysregulation and prevent neurodegenerative diseases associated with Westernized dietary patterns.

First Authors:
Hongli Shi

Correspondence Authors:
Yinghua Yu,Kuiyang Zheng,Xu-Feng Huang

All Authors:
Hongli Shi,Yinghua Yu,Danhong Lin,Peng Zheng,Peng Zhang,Minmin Hu,Qiao Wang,Wei Pan,Xiaoying Yang,Tao Hu,Qianqian Li,Renxian Tang,Feng Zhou,Kuiyang Zheng,Xu-Feng Huang

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