[Relationship between glucose metabolic disorders and expression of insulin receptor in posthepatitic cirrhosis hepatocyte and HBV DNA in pancreatic cells].
[Relationship between glucose metabolic disorders and expression of insulin receptor in posthepatitic cirrhosis hepatocyte and HBV DNA in pancreatic cells].
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发表时间：
2003-12
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通讯作者：
D. Shi;C. Dong;Li Lu;W. Cong;Yan Zhou
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作者：
D. Shi;C. Dong;Li Lu;W. Cong;Yan Zhou
目的探讨肝炎后肝硬化肝细胞胰岛素受体（IR）、酪氨酸蛋白激酶（TPK）表达及胰腺细胞HBV DNA表达与糖代谢紊乱的关系。方法采用地高辛标记探针原位杂交技术检测12例乙型肝炎肝硬化患者血清HBV标志物阳性的肝、胰腺组织中HBV DNA。应用免疫组织化学图像分析仪对12例血清HBV标志物阳性的肝炎后肝硬化患者肝细胞IR和TPK进行定量分析。免疫荧光组织化学双染法。激光共聚焦扫描显微镜下观察HBsAg和IR。结果12例肝硬化患者中有11例发生肝硬化。肝细胞HBVDNA阳性，其中糖耐量减低（IGT）7例（7/7），糖耐量正常（NGT）4例（4/5）。12例胰腺细胞中8例HBV DNA阳性，其中IGT 7例，而NGT-HBV DNA阳性者仅1例（1/5），IGT组明显多于NGT组IGT组肝细胞IR、TPK含量明显低于NGT组（P < 0.01）（P <0.01）。肝硬化肝细胞IR量与TPK密切相关，r=0.82597（P <0.01）。HBV DNA主要定位于肝细胞、胰腺腺泡细胞和胰岛细胞核内。免疫荧光组织化学双染显示HBsAg部分定位于肝细胞和胰岛细胞IR阳性区域。结论HBV可侵入胰腺腺泡细胞和胰岛细胞，这可能是HBV感染后胰岛素依赖型糖尿病样紊乱和胰岛素缺乏的直接原因。IR和TPK降低可能是肝炎或肝炎后肝硬化后发生非胰岛素依赖型糖尿病样疾病的主要原因。
OBJECTIVE To investigate relationship between glucose metabolic disorders and expression of insulin receptor (IR) and tyrosine protein kinase (TPK) in posthepatitic cirrhosis hepatocyte and HBV DNA expression in pancreatic cells. METHODS To detect HBV DNA in paraffin-embedded pancreatic and hepatic tissues from 12 posthepatitic cirrhosis patients with positive serum HBV markers by using in situ hybridization (ISH) with a digoxigenin labelled probe. The amount of IR and TPK have been evaluated by immunohistochemical quantitative analysis using image analyzer in hepatocyte of 12 patients positive for HBV markers with posthepatitic cirrhosis in serum. Immunofluorescent histochemical double staining technique was used. HBsAg and IR were observed under confocal laser scanning microscope. RESULTS Eleven of 12 cirrhosis patients? hepatocytes were HBV DNA positive, including 7 patients (7/7) with impaired glucose tolerance (IGT) and 4 patients (4/5) with normal glucose tolerance (NGT). Eight of 12 pancreatic cells were HBV DNA positive, including 7 patients (7/7) with IGT, but only one patient (1/5) with NGT-HBV DNA was found positive in pancreatic cells in significantly more subjects in IGT group than in NGT group (P less than 0.01).IR and TPK amount in hepatocyte of IGT was significantly less than that of NGT patients with posthepatitic cirrhosis (P less than 0.01). IR amount was closely related to the TPK in cirrhosis hepatocyte r=0.82597(P less than 0.01). HBV DNA was mainly localized in the nuclei of hepatocyte and pancreatic acinar and islet cells. Immunofluorescent histochemical double-staining showed that HBsAg was partly localized in the IR positive areas of hepatocytes and pancreatic islet cells. CONCLUSION HBV can invade acinar cells of pancreas and islet cells, which might be a direct cause of insulin-dependent diabetes mellitus-like the disorder and insulin absence after HBV infection. Decrease of IR and TPK might be main cause of noninsulin-dependent diabetes mellitus-like disorder after having hepatitis or posthepatitic cirrhosis.