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首页> 外文期刊>Drug Design, Development and Therapy >Metformin Decreases Insulin Resistance in Type 1 Diabetes Through Regulating p53 and RAP2A in vitro and in vivo
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Metformin Decreases Insulin Resistance in Type 1 Diabetes Through Regulating p53 and RAP2A in vitro and in vivo

机译：二甲双胍通过在体外和体内调节p53和Rap2a，降低1型糖尿病中的胰岛素抗性

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Purpose: Patients with type 1 diabetes (T1D) are associated with a high risk of multiple complications, so the development of T1D treatment is urgently needed. This study was set out to explore the molecular mechanism of metformin in the treatment of T1D insulin resistance. Patients and Methods: Subcutaneous adipose tissues were collected from 68 T1D patients and 51 healthy controls. Insulin resistance model rats and cells were constructed and treated with metformin respectively. Western blot was used to detect p53 and RAP2A protein levels, and qPCR was utilized to measure p53 and RAP2A mRNA levels. SiRNA and RAP2A siRNA vectors were constructed to observe their effects on insulin resistance model cells. Results: In T1D, p53 was up-regulated, while RAP2A was down-regulated. Metformin could effectively improve insulin resistance and inflammatory response while down-regulating p53 and up-regulating RAP2A. P53 induced insulin resistance and inflammatory response by inhibiting RAP2A and promoted apoptosis. Conclusion: Metformin improves T1D insulin resistance and inflammatory response through p53/RAP2A pathway, and the regulation of p53/RAP2A pathway is conducive to improving the efficacy of metformin in the treatment of insulin resistance.
机译：目的：1型糖尿病（T1D）的患者与多重并发症的高风险有关，因此迫切需要T1D治疗的发展。本研究旨在探讨二甲双胍治疗T1D胰岛素抵抗的分子机制。患者和方法：从68名T1D患者和51例健康对照中收集皮下脂肪组织。胰岛素抵抗模型大鼠和细胞分别用二甲双胍构建和处理。 Western印迹用于检测P53和RAP2A蛋白水平，并且利用QPCR测量P53和RAP2A mRNA水平。构建siRNA和RAP2A siRNA载体以观察它们对胰岛素抵抗模型细胞的影响。结果：在T1D中，P53上调，而RAP2A被下调。二甲双胍可以有效地改善胰岛素抵抗和炎症反应，同时降低P53和Up-Consemate Rap2a。通过抑制Rap2a和促进凋亡，p53诱导胰岛素抗性和炎症反应。结论：二甲双胍通过P53 / RAP2A途径改善T1D胰岛素抵抗和炎症反应，并且P53 / RAP2A途径的调节有利于提高二甲双胍治疗胰岛素抵抗的疗效。

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