Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two Chinese hamster ovary (CHO) cell lines stably transfected with human insulin receptor cDNA, CHO-wt and CHO-mut, which express an equivalent number of normal and kinase-defective human insulin receptors, respectively, were used to assess the roles of insulin receptor tyrosine kinase activity in insulin-regulated gene expression. The effect of insulin on gene-33-promoter-driven chloramphenicol acetyltransferase (CAT), RSVLTR-driven beta-galactosidase (pRSVLTR-betagal) and SV40 late-promoter-driven hepatitis B surface antigen (pMLSV(2)HBsAg) were examined in CHO-wt and CHO-mut cells. Insulin-stimulated gene 33 promoter is 10- to 50-fold more effective in CHO-wt cells than that in parental CHO cells. However, no enhancement of insulin sensitivity of gene 33 promoter in CHO-mut cells relative to parental CHO cells was found. Similar phenomena were also observed, in that insulin regulated pRSVLTR-betagal and pMLSV(2)HBsAg in these three CHO lines. Our data indicated that the protein kinase activity of the insulin receptor is essential for the stimulatory activity of insulin toward the activities of different promoters. Copyright 1994 S. Karger AG, Basel
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PMID:Protein Kinase Activity of the Insulin Receptor Is Essential for Insulin-Regulated Gene Expression. 1172

The relationship between the GOT/GPT ratio in nonviral liver disorders and underlying physical condition and life-style were evaluated. The subjects were 12,808 male railway company workers who underwent an annual health checkup. Nonviral liver disorders were defined as elevated transaminases (GOT > 76 IU/liter or GPT > 86 IU/liter, while negative for hepatitis B and C markers (282 cases). Controls were 9,783 males with normal findings for GOT, GPT, and y-GTP. By logistic regression analysis, GOT-dominant liver disorders were significantly related to alcohol consumption, hypertriglyceridemia, and diabetes mellitus. They were still significant on multivariate analysis. GPT-dominant liver disorders were significantly related to obesity, less exercise, hypercholesterolemia, and hypertriglyceridemia. Obesity and hypercholesterolemia were significant on multivariate analysis. In conclusion, the relationship between hypertriglyceridemia or diabetes mellitus and GOT-dominant disorders, which was not explained empirically, could indicate another pathogenesis for nonviral liver disorders, such as underlying insulin resistance.
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PMID:Various S-GOT/S-GPT ratios in nonviral liver disorders and related physical conditions and life-style. 1191 40

We have shown previously that insulin suppresses the expression of hepatitis B surface antigen (HBsAg) gene from an endogenous integrated viral genome in cultured human hepatoma Hep3B cells. In this study, we demonstrated that insulin suppresses the viral mRNA transcribed from transiently transfected tandem repeat hepatitis B virus (HBV) dimer DNA or DNA fragment that contains only the major HBsAg gene. Insulin treatment also resulted in a decrease in HBV viral particles produced by the HBV-DNA-transfected cells in a dose-dependent manner. Furthermore, when insulin was simultaneously added with glucocorticoid, which stimulates HBV gene expression, the stimulatory effect of glucocorticoid was completely abolished. Our results suggest that insulin has a dominant negative effect on the HBV gene expression in cultured human liver cells.
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PMID:Insulin Dominantly Suppresses Hepatitis B Virus Gene Expression in Cultured Human Hepatoma Cells. 1238 76

Despite the abundance of reports concerning the increased frequency of diabetes and impaired glucose tolerance in chronic liver diseases, the mechanisms underlying this phenomenon have not been resolved. 30 patients with hepatitis C virus (HCV) infection and 17 with hepatitis B virus (HBV) infection who showed an altered responds to a standard oral glucose tolerance test were investigated in order to evaluate their pancreatic-endocrine features. We have also evaluated 40 patients (20 with HCV infection and 20 with HCB infection) who developed diabetes after diagnosis of liver disease. Patients with HBV infection showed signs of enhanced insulin resistance but overt diabetes develops in those who, in addition to insulin insensitivity, have a relative defect of insulin secretion. In patients with HCV infection the significantly lower plasma insulin and C-peptide levels suggest that impairment of insulin secretion is the main mechanism leading to both glucose intolerance and overt diabetes.
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PMID:[The pathological mechanisms of glycoregulation disturbances in chronic hepatitis B and C]. 1263 77

The effects of adding rosiglitazone to existing sulfonylurea (SU) treatment have not previously been studied in Chinese patients with type 2 diabetes and no known pre-existing hepatic impairment. Patients were randomized to receive rosiglitazone 2 mg twice daily (R4 + SU) or 4 mg twice daily (R8 + SU) or placebo (SU + P) for 24 weeks in addition to existing SU treatment. Most patients were taking concomitant glibenclamide (34%) or gliclazide (25%). Changes in glycosylated hemoglobin (HbA(1c)), fasting plasma glucose (FPG), and plasma insulin concentrations were measured. Of the 530 patients enrolled (45% male, mean age 59 years), 105 were in the SU + P group, 215 in the R4 + SU group, and 210 in the R8 + SU group. The mean baseline HbA(1c) was 9.8%, and FPG was 183.8 mg/dL. Compared with placebo, addition of rosiglitazone (2 or 4 mg twice daily) produced significant decreases in mean HbA(1c) (1.04% and 1.44%, respectively; p < 0.0001) and FPG (21.6 and 36.0 mg/dL, respectively; p < 0.0001). There were statistically significant (p < 0.0001) reductions from baseline in insulin concentration of 23.3 and 30.4 pmol/L in the R4 + SU and R8 + SU groups, respectively. Despite the high prevalence of seropositivity for hepatitis B and/or C at baseline (56%), there was no evidence of hepatotoxicity. No clinically significant changes in routine hematology, biochemistry, or electrocardiogram were observed. The addition of rosiglitazone to SU produced clinically significant improvements in glycemic control in Chinese patients with type 2 diabetes. Rosiglitazone plus SU was well tolerated irrespective of hepatitis B and C serological status.
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PMID:Addition of rosiglitazone to existing sulfonylurea treatment in chinese patients with type 2 diabetes and exposure to hepatitis B or C. 1272 6

Disulfide reduction is an important step in antigen processing for HLA class II restricted T cell responses. Migration inhibitory factor (MIF) is a member of the thioredoxin family and has been classically defined as a cytokine. Using enzyme-linked immunosorbent assay and CD analysis, here we describe the binding to MIF of two peptides, hepatitis B surface antigen (HBsAg) and insulin B (InsB) with high affinity for HLA class II allo-types, HLA-DP2 and HLA-DQ8, respectively. At neutral pH, cysteinylated InsB was a substrate for MIF thiol reductase activity, as assessed by mass spectroscopy/electrospray analysis. Finally, a biologically active form of MIF co-immunopurified with mature forms of HLA DP2/15, and a peptide derived from the HLA-DP beta1 helix could be used for affinity purification of MIF. The possibility that MIF participates in class II antigen presentation and/or as a chaperone is discussed.
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PMID:Molecular interaction and enzymatic activity of macrophage migration inhibitory factor with immunorelevant peptides. 1274 Mar 74

Chronic liver disease is a major cause of morbidity and mortality in the United States. Although often used to detect liver disease, the prevalence and etiology of elevated aminotransferases are unknown. We analyzed data on adults ages 17 yr and older (N = 15,676) from the Third National Health and Nutrition Examination Survey (1988-1994). Participants were classified as having elevated aminotransferase levels if either aspartate aminotransferase or alanine aminotransferase was elevated above normal. Aminotransferase elevation was classified as "explained" if there was laboratory evidence of hepatitis B or C infection, iron overload, or if there was a history of alcohol consumption. Analyses were weighted to provide national estimates. The prevalence of aminotransferase elevation in the United States was 7.9%. Aminotransferase elevation was more common in men compared to women (9.3% vs 6.6%, p = 0.002), in Mexican Americans (14.9%) and non-Hispanic blacks (8.1%) compared to non-Hispanic whites (7.1%, p < 0.001). High alcohol consumption, hepatitis B or C infection and high transferrin saturation were found in only 31.0% of cases. Aminotransferase elevation was unexplained in the majority (69.0%). In both men and women, unexplained aminotransferase elevation was significantly associated with higher body mass index, waist circumference, triglycerides, fasting insulin, and lower HDL; and with type 2 diabetes and hypertension in women (all p < 0.05). Aminotransferase elevation was common in the United States, and the majority could not be unexplained by alcohol consumption, viral hepatitis or hemochromatosis. Unexplained aminotransferase elevation was strongly associated with adiposity and other features of the metabolic syndrome, and thus may represent nonalcoholic fatty liver disease.
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PMID:The prevalence and etiology of elevated aminotransferase levels in the United States. 1280 14

Hepatitis B virus (HBV) is the major cause of chronic liver disease and hepatocellular carcinoma in the world, with more than 400 million people infected worldwide. To date, there is no reliable model for the study of the many aspects of HBV infection, despite the use of the chimpanzee. Although several alternative methods have been previously developed for the in vitro study of HBV infection, there is still an urgent need for new in vitro infection models, including for the ability of HBV to integrate into the host cell genome. Here we describe a process to improve infection of the human hepatoma cell lines HepG2 and HuH-7 in vitro with HBV originating from human blood. As shown previously for infection of hepatocytes with hepatitis C virus (HCV), the removal of the cell-bound lipoproteins prior to the addition of the viral inoculum to the cells could also be critical for the uptake of HBV via lipoprotein (LDL)-related receptors. Induction by insulin and dexamethasone led to an increase of HBsAg expression at the cell surface in association with the integration of the viral DNA into the host genome and HBx RNA detection. This integration process was also shown to be associated with cytopathic changes and further phenotypic transformations of the cells.
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PMID:Latent hepatitis B virus (HBV) infection and HBV DNA integration is associated with further transformation of hepatoma cells in vitro. 1294 86

Hepatitis B virus-infected patients secrete enormous quantities (50-300 microg/ml) of hepatitis B surface antigen (HBsAg) in their serum. One hypothesis for this synthetic effort is that these lipoprotein particles serve to adsorb neutralizing antisurface antibodies. We have shown that insulin suppresses the expression of HBsAg in human hepatoma cell Hep3B cells. We further studied the signaling pathway of insulin on the inhibition of HBsAg. Using a fungal metabolite, lovastatin, to block the p21Ras signaling pathway of insulin, we found that lovastatin inhibited the secretion of HBsAg into culture medium in Hep3B cells; however, the involvement of p21Ras-MAPKs was excluded in this effect. The cholesterol depletion from the membrane, leading to the destabilization of rafts, was the mechanism for the lovastatin inhibition of HBsAg secretion. However, lovastatin has no effect on the secretion of infectious viral Dane particles. Herein, we show for the first time that cholesterol is required for HBsAg secretion.
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PMID:Cholesterol requirement of hepatitis B surface antigen (HBsAg) secretion. 1451 78

The management of chronic viral hepatitis has changed significantly with the availability of effective antiviral agents. There is now a high probability that timely intervention can arrest development of cirrhosis, thereby preventing mortality from portal hypertension, liver failure and liver cancer. This two-part review discusses the implications of this new era of antiviral therapy for physicians. The present review is about chronic hepatitis C virus (HCV); a similar review that considers the treatment of hepatitis B virus will be published in a later issue of the Internal Medicine Journal. Chronic HCV infection is common, but fibrotic progression of liver disease is slow and variable; many infected persons never develop cirrhosis. Case selection for antiviral therapy is crucial. The most effective therapy is a pegylated (long-acting) interferon with ribavirin. Sustained viral response (SVR) (absent viraemia 6 months after completing treatment) can be obtained in 40-60% of individuals infected with genotype 1 and in approximately 67% with genotype 4 after 12 months of treatment. Response rates are higher (75-85%) with genotypes 2 and 3 after only 6 months of treatment. Late relapse is negligible after SVR. This viral cure reverses hepatic fibrosis, reduces the risk of liver failure and of hepato-cellular carcinoma. Combination therapy requires a supportive setting to minimize the impact of side-effects and maximize therapeutic effectiveness. Overall management of HCV-infected persons must also embrace measures to improve quality of life by preventing or dealing with psychosocial issues and advocating lifestyle changes to counter comorbidity from alcohol, central obesity and insulin resistance. These latter factors favour fibrotic disease progression, complications of cirrhosis (such as hepatocellular carcinoma) and development of type 2 diabetes mellitus, as well as eroding the chances of SVR with antiviral therapy.
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PMID:Management of chronic hepatitis C virus infection: a new era of disease control. 1522 94


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