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目的:探讨糖尿病患者肝脏与正常对照肝脏基因表达谱的变化,并进行代谢通路生物信息学分析。方法:应用Affymetrix的Human Genome U133A array芯片检测糖尿病肝脏组织(n=2)和正常对照肝脏组织(n=2)的基因表达谱变化,通过DAVID分析平台对芯片监测到的表达上调的基因进行KEGG通路分析,并用RT-PCR验证部分基因的表达情况。结果:以比值大于2或小于-2为准,共有492条基因明显上调,820条基因明显下调;在差异表达明显的前20位基因中,涉及氧化应激、免疫炎症反应和脂代谢。KEGG代谢通路分析显示:该差异表达基因谱符合2型糖尿病的发病机制,其差异表达明显基因的代谢通路涉及胰岛素信号通路、脂代谢、补体和凝血系统、糖代谢、粘附功能和细胞因子和受体的相互作用,RT-PCR证实差异表达明显基因SOD2mRNA和CRPmRNA确实表达明显上调。结论:糖尿病肝脏与正常肝脏组织基因表达谱的变化在代谢通路上主要表现为在糖、脂代谢和胰岛素信号通路、补体和凝血系统等的改变,肝脏在糖尿病发病机制中的作用可能与其参与糖脂代谢和胰岛素的作用异常有关。
Objective: To investigate the changes of gene expression profiles in the liver and normal control liver of diabetic patients, and to analyze the metabolic pathways by bioinformatics. Methods: The gene expression profile of diabetic liver tissue (n = 2) and normal control liver tissue (n = 2) was detected by Affymetrix Human Genome U133A array. The gene whose expression was up-regulated was detected by DAVID analysis platform. Pathway analysis, and use RT-PCR to verify the expression of some genes. RESULTS: With a ratio greater than 2 or less than 2, a total of 492 genes were significantly up-regulated and 820 genes were significantly down-regulated. Among the top 20 differentially expressed genes, oxidative stress, immune-inflammatory responses and lipid metabolism were involved. KEGG metabolic pathway analysis showed that the differentially expressed gene profile was found to be associated with the pathogenesis of type 2 diabetes. The differentially expressed genes involved in the metabolic pathways involved in insulin signaling, lipid metabolism, complement and coagulation systems, glycometabolism, adhesion and cytokines Receptor interaction, RT-PCR confirmed that differentially expressed genes SOD2 mRNA and CRP mRNA did indeed significantly up-regulated. CONCLUSION: The changes of gene expression profile in the liver and normal liver of diabetic rats are mainly manifested by changes in glucose and lipid metabolism, insulin signaling pathway, complement and coagulation system, and the role of liver in the pathogenesis of diabetes. Lipid metabolism and the abnormal effects of insulin.