CINTESIS - Centre for Research in Health Technologies and Information Systems, Porto, Portugal.
Nutrition & Metabolism, NOVA Medical School, Faculdade de Ciências Médicas, Universidade Nova de Lisboa, Lisboa, Portugal.
Sci Rep. 2018 Jul 27;8(1):11341. doi: 10.1038/s41598-018-29744-5.
High-fat (HF) diets are thought to disrupt the profile of the gut microbiota in a manner that may contribute to the neuroinflammation and neurobehavioral changes observed in obesity. Accordingly, we hypothesize that by preventing HF-diet induced dysbiosis it is possible to prevent neuroinflammation and the consequent neurological disorders. Anthocyanins are flavonoids found in berries that exhibit anti-neuroinflammatory properties in the context of obesity. Here, we demonstrate that the blackberry anthocyanin-rich extract (BE) can modulate gut microbiota composition and counteract some of the features of HF-diet induced dysbiosis. In addition, we show that the modifications in gut microbial environment are partially linked with the anti-neuroinflammatory properties of BE. Through fecal metabolome analysis, we unravel the mechanism by which BE participates in the bilateral communication between the gut and the brain. BE alters host tryptophan metabolism, increasing the production of the neuroprotective metabolite kynurenic acid. These findings strongly suggest that dietary manipulation of the gut microbiota with anthocyanins can attenuate the neurologic complications of obesity, thus expanding the classification of psychobiotics to anthocyanins.
高脂肪(HF)饮食被认为以某种方式破坏了肠道微生物群的特征,而这种破坏可能导致肥胖症中观察到的神经炎症和神经行为的改变。因此,我们假设通过预防 HF 饮食引起的微生态失调,可以预防神经炎症和随之而来的神经紊乱。花色苷是存在于浆果中的类黄酮,在肥胖的情况下具有抗神经炎症的特性。在这里,我们证明黑莓花色苷丰富的提取物(BE)可以调节肠道微生物群的组成,并对抗 HF 饮食引起的微生态失调的某些特征。此外,我们还表明,肠道微生物环境的改变与 BE 的抗神经炎症特性部分相关。通过粪便代谢组学分析,我们揭示了 BE 参与肠道和大脑之间双向通讯的机制。BE 改变了宿主色氨酸代谢,增加了神经保护代谢物犬尿氨酸的产生。这些发现强烈表明,用花色苷对肠道微生物群进行饮食干预可以减轻肥胖引起的神经并发症,从而将益生菌的分类扩展到花色苷。