小岛
点头
点头老鼠
2型糖尿病
糖尿病
炎症
转录组
内分泌学
内科学
1型糖尿病
免疫系统
医学
胰岛素
β细胞
生物
免疫学
基因表达
基因
生物化学
作者
Xiangqian Li,Lina Wang,Gang Ma,Xiaoling Chen,Shushu Yang,Mengjun Zhang,Zhengni Zheng,Jie Zhou,Lingjuan Zhu,Yuzhang Wu,Li Wang
标识
DOI:10.3389/fendo.2022.1037822
摘要
Introduction Epidemiological studies have suggested that dietary factors, especially high consumption of high glycaemic index carbohydrates and sugars, may trigger or exacerbate the progression of type 1 diabetes. We aimed to provide experimental evidence to confirm this relevance and to explore the underlying mechanisms. Methods NOD mice were given sustained high-glucose drinking or glucose-free water and observed for the incidence of type 1 diabetes and islet inflammation. RNAseq was performed to detect the transcriptome changes of the NOD islet beta cell line NIT-1 after high glucose treatment, and mass spectrometry was performed to detect the proteome changes of NIT-1-cells-derived sEVs. Results Sustained high glucose drinking significantly aggravates islet inflammation and accelerates the onset of type 1 diabetes in NOD mice. Mechanistically, high glucose treatment induces aberrant ER stress and up-regulates the expression of autoantigens in islet beta cell. Moreover, high glucose treatment alters the proteome of beta-cells-derived sEVs, and significantly enhances the ability of sEVs to promote DC maturation and stimulate immune inflammatory response. Discussion This study provides evidence for negative effect of high glucose intake as a dietary factor on the pathogenesis of type 1 diabetes in genetically predisposed individuals. Therefore, avoiding high sugar intake may be an effective disease prevention strategy for children or adults susceptible to type 1 diabetes.
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