首页|熟小米醇溶蛋白改善糖尿病小鼠血糖代谢紊乱的分子机制

熟小米醇溶蛋白改善糖尿病小鼠血糖代谢紊乱的分子机制

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目的:基于肝脏转录组学分析熟小米醇溶蛋白改善糖代谢的分子机制.方法:采用转录组学技术检测熟小米干预后糖尿病小鼠肝脏基因的表达图谱变化.结果:与模型组小鼠相比,熟小米醇溶蛋白干预引起小鼠肝脏中1 758个基因显著上调,198个基因显著下调.表明熟小米醇溶蛋白的干预显著改变了糖尿病小鼠的肝脏基因表达谱.经KEGG功能注释分析,发现熟小米醇溶蛋白干预后改变的差异基因主要聚集在与脂质代谢和碳水化合物代谢相关的通路上.对差异基因进行KEGG通路富集分析,结果显示磷脂酰肌醇3-激酶/蛋白激酶B信号通路是富集最显著的糖代谢相关信号通路,其中包含27个显著上调和1个显著下调的差异基因.本研究旨在阐明熟小米醇溶蛋白发挥降糖作用的分子机制,为开发针对糖尿病或者血糖异常人群的功能食品提供基础数据.
Molecular Mechanism of Cooked Foxtail Millet Prolamin in Improving Glucose Metabolism Disorder in Diabetes Mice
Previous studies have shown that prolamin from cooked foxtail millet(PCFM)can effectively improve glucose metabolism disturbances in high-fat diet and streptozotocin-induced diabetic mice.The current study aimed to investigate the molecular mechanism by which PCFM enhances glucose metabolism,focusing on liver transcriptomics.The results showed that,compared to the control group,the livers of mice treated with PCFM exhibited significant up-regulation of 1 758 differentially expressed genes and down-regulation of 198 genes.KEGG functional annotation analysis revealed that these genes were associated with pathways related to lipid and carbohydrate metabolism.Furthermore,the KEGG pathway enrichment analysis highlighted the phosphoinositide-3 kinase(PI3K)/protein kinase B(AKT)signaling pathway as the most significantly enriched pathway involved in glucose metabolism,with 27 genes up-regulated and one down-regulated after PCFM intervention.This study aims to elucidate the molecular mechanisms underlying the hypoglycemic effects of PCFM and provide a foundation for the development of functional foods targeting hypoglycemia.

foxtail milletprolamintranscriptomedifferential genePI3K/AKT signaling pathway

付永霞、张凡、刘振宇、王晗、郭尚、沈群

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山西农业大学 山西功能食品研究院 太原 030031

中国农业大学食品科学与营养工程学院 国家粮食产业(青稞深加工)技术创新中心植物蛋白与谷物加工北京市重点实验室 国家果蔬加工工程技术研究中心 北京 100083

北京一轻研究院有限公司 北京 101111

四川大学轻工科学与工程学院 成都 610065

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小米 醇溶蛋白 转录组学 差异基因 磷脂酰肌醇3-激酶/蛋白激酶B信号通路

国家现代农业产业技术体系

CARS-07-13.5

2024

中国食品学报
中国食品科学技术学会

中国食品学报

CSTPCD北大核心EI
影响因子:1.079
ISSN:1009-7848
年,卷(期):2024.24(7)
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