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首页> 外文期刊>Cell biology international. >Regulation of insulin resistance by targeting the insulin‐like growth factor 1 receptor with microRNA‐122‐5p in hepatic cells
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Regulation of insulin resistance by targeting the insulin‐like growth factor 1 receptor with microRNA‐122‐5p in hepatic cells

机译：通过在肝细胞中靶向胰岛素样生长因子1受体来调节胰岛素样生长因子1受体。肝细胞中微小RONA-122-5P

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Abstract Insulin resistance (IR) is a common etiology of type 2 diabetes (T2D) defined by a state of decreased reactivity to insulin in multiple organs, such as the liver. This study aims to investigate how microRNA‐122‐5p (miR‐122) regulates the hepatic IR in vitro. We first found that the miR‐122 level was upregulated in the liver of rats fed with a high‐fat diet and injected with streptozotocin (T2D rats), while the expression level of insulin‐like growth factor 1 receptor (IGF‐1R), a potential target of miR‐122, was downregulated in the diabetic liver. In vitro, glucosamine‐induced IR was introduced in HepG2 hepatic cells, and the levels of miR‐122 and IGF‐1R were further assessed. An increase of miR‐122 level and a decrease of IGF‐IR level were observed in IR hepatic cells, which was?the same as that in the diabetic liver. Results of the luciferase reporter assay validated IGF‐1R as a direct target of miR‐122. Moreover, in IR HepG2 cells, antagonizing miR‐122 with its specific inhibitor enhanced glucose uptake and suppressed the expression of glucose 6‐phosphatase and phosphoenolpyruvate carboxykinase, two key enzymes in regulating gluconeogenesis. Such alterations induced by the miR‐122 inhibitor in IR hepatic cells were impaired when IGF‐1R was simultaneously knocked down. In addition, the PI3K/Akt pathway was deactivated in IR cells, and then reactivated with miR‐122 inhibitor transfection. In conclusion, our study demonstrates that miR‐122 is able to regulate IR in hepatic cells by targeting IGF‐1R .
机译：摘要胰岛素抵抗（IR）是由多个器官中的胰岛素的反应性降低的2型糖尿病（T2D）的常见病因，例如肝脏。本研究旨在研究MicroRNA-122-5P（MIR-122）如何调节肝红外体外。首先发现，用高脂饮食喂养的大鼠肝脏并注射链脲佐菌素（T2D大鼠），同时胰岛素样生长因子1受体（IGF-1R）的表达水平上调miR-122水平。 miR-122的潜在靶标在糖尿病肝脏中下调。体外，在HepG2肝细胞中引入葡糖胺诱导的IR，进一步评估miR-122和IGF-1R的水平。在IR肝细胞中观察到miR-122水平的增加和IGF-IR水平的降低，这是与糖尿病肝脏中的相同。荧光素酶报告结果测定的结果验证了IGF-1R作为MiR-122的直接靶标。此外，在IR HepG2细胞中，用其特异性抑制剂增强葡萄糖摄取和抑制葡萄糖6-磷酸酶和磷酸丙酮酸羧基酶，两个关键酶在调节葡糖生成中的表达。当IGF-1R同时敲下来时，MiR-122抑制剂在IR肝细胞中诱导的这种改变受到损害。另外，在IR细胞中停用PI3K / AKT途径，然后用miR-122抑制剂转染重新激活。总之，我们的研究表明MIR-122能够通过靶向IGF-1R来调节肝细胞中的IR。

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