[Relationship between glucose metabolic disorders and expression of insulin receptor in posthepatitic cirrhosis hepatocyte and HBV DNA in pancreatic cells].
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.


CONCLUSIONS
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.
Shi
De-ren
DR
Department of Infection, No.201 Hosptal of PLA, Liao yang 111000, China.
Dong
Chuan-ling
CL
Lu
Li
L
Cong
Wen-tian
WT
Zhou
Yan
Y
D004279:DNA, Viral / Q000032:analysis*; D005260:Female; D044882:Glucose Metabolism Disorders / Q000150:complications / Q000378:metabolism* / Q000821:virology; D006515:Hepatitis B virus / Q000235:genetics*; D022781:Hepatocytes / Q000378:metabolism* / Q000821:virology; D006801:Humans; D017403:In Situ Hybridization; D008103:Liver Cirrhosis / Q000150:complications / Q000378:metabolism* / Q000821:virology; D008297:Male; D008875:Middle Aged; D010179:Pancreas / Q000166:cytology / Q000821:virology*; D011505:Protein-Tyrosine Kinases / Q000378:metabolism; D011972:Receptor, Insulin / Q000378:metabolism*
D004279:DNA, Viral; D011505:Protein-Tyrosine Kinases; D011972:Receptor, Insulin