胰岛素信号转导与胰岛素抵抗的研究进展

发布时间：2018-06-01 00:44

本文选题：2型糖尿病 + 胰岛素抵抗　；参考：《河北医科大学》2017年硕士论文

【摘要】：2型糖尿病是一种由胰岛素分泌不足和胰岛素抵抗(IR)引起的以慢性高血糖为特征的代谢性疾病,其中IR为最重要的病理机制。胰岛素信号转导通路的异常在IR的发生、发展中起到关键性作用。胰岛素与其分布在肝脏、脂肪组织、骨骼肌等靶组织表面受体结合后,使受体底物蛋白酪氨酸残基磷酸化而激活,之后信号转导通路会发生一系列磷酸化级联反应完成胰岛素信号在靶组织细胞内逐级传递并瀑布样放大,从而产生多种生物学效应。常见的胰岛素信号转导通路有:磷脂酰肌醇-3激酶(PI3K)通路和促分裂原活化蛋白激酶(MAPK)通路,当由于肥胖、氧化应激、内质网应激等各种原因,使通路中任何位点出现异常,均会导致胰岛素抵抗。本文就胰岛素信号转导异常的研究进展进行综述。
[Abstract]:Type 2 diabetes is a metabolic disease characterized by chronic hyperglycemia and insulin resistance (IR), of which IR is the most important pathological mechanism. The abnormal insulin signal transduction pathway plays a key role in the development of IR. Islet is distributed in the liver, adipose tissue, and skeletal muscle. After the binding of the target tissue surface receptor, the receptor substrate protein tyrosine residues are phosphorylated and activated. After that, a series of phosphorylation cascade reactions will occur in the signal transduction pathway to complete the insulin signal in the target tissue cell by step by step and the waterfall sample enlargement, thus producing a variety of biological effects. The lipooyl inositol -3 kinase (PI3K) pathway and mitogen activated protein kinase (MAPK) pathway, when due to obesity, oxidative stress, and endoplasmic reticulum stress, make any site abnormal in the pathway and lead to insulin resistance. This article reviews the progress in the study of insulin signal transduction heterogeneity.
【学位授予单位】：河北医科大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R587.1

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