Protein Isolates from Raw and Cooked Foxtail Millet Attenuate Development of Type 2 Diabetes in Streptozotocin-Induced Diabetic Mice

文献类型： 外文期刊

第一作者： Fu, Yongxia

作者： Fu, Yongxia;Yin, Ruiyang;Xue, Yong;Shen, Qun;Fu, Yongxia;Yin, Ruiyang;Xue, Yong;Shen, Qun;Fu, Yongxia;Yin, Ruiyang;Xue, Yong;Shen, Qun;Guo, Erhu;Cheng, Ruhong;Diao, Xianmin

作者机构：

关键词： foxtail millet; GLP-1R/PI3K/AKT pathway; gut microbiota; protein isolate; type 2 diabetes

期刊名称：MOLECULAR NUTRITION & FOOD RESEARCH （ 影响因子：5.914； 五年影响因子：6.409 ）

ISSN： 1613-4125

年卷期： 2021 年 65 卷 6 期

页码：

收录情况： SCI

摘要： Scope: Millet protein has received much attention due to its beneficial role in alleviating metabolic disease symptoms. This study aims to investigate the role and molecular mechanism of foxtail millet protein isolates, including protein isolates from raw and cooked foxtail millet in alleviating diabetes, including gut microbiota and intracellular signal pathways. Methods and results: Protein isolates from raw and cooked foxtail millet are orally administered to streptozotocin (STZ)-induced diabetic mice for 5 weeks before hypoglycemic effect evaluation. The results show that foxtail millet protein isolates improve glucose intolerance and insulin resistance in diabetic mice. However, only the protein isolate from cooked foxtail millet reverse the weight loss trend and alleviate lipid disorders in diabetic mice. Besides, 16S rRNA sequencing show that both raw and cooked foxtail millet protein isolates altered diabetes-induced gut dysbiosis. In addition, western blotting analysis indicated that the protein isolate from cooked foxtail millet increases the expression levels of glucagon-like peptide-1 receptor (GLP-1R), phosphoinositide 3-kinase (PI3K), and phosphoinositide-protein kinase B (p-AKT)/AKT while the protein isolate from raw foxtail millet downregulates stearoyl-coenzyme A desaturase 1 (SCD1) level. Conclusion: Both raw and cooked foxtail millet protein isolates can exert hypoglycemic effects in diabetic mice through rewiring glucose homeostasis, mitigating diabetes-induced gut dysbiosis, and affecting the GLP-1R/PI3K/AKT pathway.

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