胰岛素抵抗肝细胞多药耐药基因mdr1的表达
he expression of multi-drug resitance gene 1 in insulin-resistant hepatic cells
目的：体外观察肝细胞诱导发生胰岛素抵抗（Insulin resistance, IR）中多药耐药基因mdr1的表达。 方法：采用高浓度胰岛素诱发肝源性细胞HepG2建立IR细胞模型（HepG2 IR细胞），GOD-POD微量化法测定葡萄糖消耗量，RT-PCR检测胰HepG2 IR细胞mdr1基因和胰岛素受体（Insulin receptor, InsR）mRNA的表达，流式细胞术（FCM）检测P-糖蛋白（P-glycoprotein，P-gp）和InsR蛋白水平。结果：胰岛素诱发HepG2发生IR后，HepG2 IR细胞葡萄糖消耗量降低约10%~45%，InsR基因mRNA表达显著下调、受体表达量降低50.2%-82.9%。胰岛素诱导HepG2细胞产生抗性的过程中，耐药基因mdr1基因表达同步显著增强，mRNA转录增高0.7-2.1倍，P-gp表达阳性细胞增加0.6-1.7倍、表达强度增高。结论：胰岛素诱发的肝脏胰岛素抵抗细胞mdr1基因和P-gp的表达显著增强，提示耐药基因可能与胰岛素抵抗相关联。
OBJECTIVE: To explore the expression of multidrug resistance 1(mdr1) gene during induction of insulin resistance of hepatic cells. METHODS: Insulin-resistant Hepg2 cell model (IR-HepG2) was induced using high concentration of insulin. The change in glucose consumption was detected with a GOD-POD assay. The expression of mdr1 and insulin receptor(InsR) gene mRNA was assessed by reverse transcription RCR(RT-PCR). Expression of P-gp and InsR protein was measured with flow cytometry (FCM). RESULTS: The glucose consumption was decresed by 10％-45％ in IR-HepG2 cells compared with HepG2 cells. The expression of InsR mRNA and protein was reduced by 16.7%-49.7% and 50.2%-82.9%, respectively. At the same time, the expression of mdr1 gene up-regulated significantly, and mdr1 mRNA increased by 0.7-2.1 folds and P-gp positive cells by 0.6-1.7 folds. CONCLUSION: The expression of mdr1/P-gp in insulin-resistant hepatocytes induced by insulin is enhanced significantly, it is strongly suggest that drug resistance gene mdr1 and P-gp may participates in the process of insulin resistance.
陈静、魏虎来、李林静、程杰、马艳云
基础医学生物科学研究方法、生物科学研究技术生理学
胰岛素抵抗HepG2细胞多药耐药基因1（mdr1）
Insulin resistanceHepatic cellMultidrug resistance gene 1
陈静,魏虎来,李林静,程杰,马艳云.胰岛素抵抗肝细胞多药耐药基因mdr1的表达[EB/OL].(2008-01-11)[2025-07-21].http://www.paper.edu.cn/releasepaper/content/200801-385.点此复制
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