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狐尾粟通过肠道微生物介导的 PI3K/AKT 和 NF-κB 信号通路改善糖尿病大鼠的血糖代谢。

Foxtail Millet Improves Blood Glucose Metabolism in Diabetic Rats through PI3K/AKT and NF-κB Signaling Pathways Mediated by Gut Microbiota.

机构信息

Beijing Advanced Innovation Center for Food Nutrition and Human Health, Beijing Engineering and Technology Research Center of Food Additives, Beijing Technology and Business University, Beijing 100048, China.

Key Laboratory of Plant Protein and Grain Processing, National Engineering and Technology Research Center for Fruits and Vegetables, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083, China.

出版信息

Nutrients. 2021 May 27;13(6):1837. doi: 10.3390/nu13061837.

DOI:10.3390/nu13061837
PMID:34072141
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8228963/
Abstract

Foxtail millet (FM) is receiving ongoing increased attention due to its beneficial health effects, including the hypoglycemic effect. However, the underlying mechanisms of the hypoglycemic effect have been underexplored. In the present study, the hypoglycemic effect of FM supplementation was confirmed again in high-fat diet and streptozotocin-induced diabetic rats with significantly decreased fasting glucose (FG), glycated serum protein, and areas under the glucose tolerance test ( < 0.05). We employed 16S rRNA and liver RNA sequencing technologies to identify the target gut microbes and signaling pathways involved in the hypoglycemic effect of FM supplementation. The results showed that FM supplementation significantly increased the relative abundance of Lactobacillus and Ruminococcus_2, which were significantly negatively correlated with FG and 2-h glucose. FM supplementation significantly reversed the trends of gene expression in diabetic rats. Specifically, FM supplementation inhibited gluconeogenesis, stimulated glycolysis, and restored fatty acid synthesis through activation of the PI3K/AKT signaling pathway. FM also reduced inflammation through inhibition of the NF-κB signaling pathway. Spearman's correlation analysis indicated a complicated set of interdependencies among the gut microbiota, signaling pathways, and metabolic parameters. Collectively, the above results suggest that the hypoglycemic effect of FM was at least partially mediated by the increased relative abundance of Lactobacillus, activation of the PI3K/AKT signaling pathway, and inhibition of the NF-κB signaling pathway.

摘要

黍米(FM)因其有益健康的作用,包括降血糖作用,正受到越来越多的关注。然而,其降血糖作用的潜在机制仍未得到充分探索。在本研究中,FM 补充剂在高脂肪饮食和链脲佐菌素诱导的糖尿病大鼠中再次证实了其降血糖作用,显著降低了空腹血糖(FG)、糖化血清蛋白和葡萄糖耐量试验下的面积(<0.05)。我们采用 16S rRNA 和肝 RNA 测序技术,鉴定了参与 FM 补充剂降血糖作用的靶向肠道微生物和信号通路。结果表明,FM 补充剂显著增加了乳酸杆菌和 Ruminococcus_2 的相对丰度,它们与 FG 和 2-h 葡萄糖呈显著负相关。FM 补充剂显著逆转了糖尿病大鼠的基因表达趋势。具体而言,FM 补充剂通过激活 PI3K/AKT 信号通路抑制糖异生,刺激糖酵解,并恢复脂肪酸合成。FM 还通过抑制 NF-κB 信号通路减轻炎症。Spearman 相关性分析表明,肠道微生物群、信号通路和代谢参数之间存在着复杂的相互依存关系。综上所述,上述结果表明,FM 的降血糖作用至少部分是通过增加乳酸杆菌的相对丰度、激活 PI3K/AKT 信号通路和抑制 NF-κB 信号通路来介导的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0e0/8228963/1cdb37bb71f8/nutrients-13-01837-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0e0/8228963/5d8f5631cb35/nutrients-13-01837-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0e0/8228963/e36c73a0e088/nutrients-13-01837-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0e0/8228963/55baae7d5105/nutrients-13-01837-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0e0/8228963/f3b205f640d8/nutrients-13-01837-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0e0/8228963/2eafea2c6018/nutrients-13-01837-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0e0/8228963/69b4d0c001f4/nutrients-13-01837-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0e0/8228963/d4be4fb25066/nutrients-13-01837-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0e0/8228963/1cdb37bb71f8/nutrients-13-01837-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0e0/8228963/5d8f5631cb35/nutrients-13-01837-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0e0/8228963/e36c73a0e088/nutrients-13-01837-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0e0/8228963/55baae7d5105/nutrients-13-01837-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0e0/8228963/f3b205f640d8/nutrients-13-01837-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0e0/8228963/2eafea2c6018/nutrients-13-01837-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0e0/8228963/69b4d0c001f4/nutrients-13-01837-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0e0/8228963/d4be4fb25066/nutrients-13-01837-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0e0/8228963/1cdb37bb71f8/nutrients-13-01837-g008.jpg

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