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

The association of viral hepatitis and acute pancreatitis is well described in the literature. Most of the cases occur in conjunction with fulminant hepatitis A and hepatitis B virus infections. The recent literature reports increasing number of cases of this complication secondary to hepatitis E virus (HEV) infection, mostly in young adults in regions endemic for the virus. Till date, to the authors' knowledge, there are 14 well-documented cases of HEV-associated acute pancreatitis in the literature. This study reports on a 7-year-old boy from India deficient in glucose 6 phosphate dehydrogenase (G6PD) with moderately severe pancreatitis, manifesting during the course of nonfulminant acute HEV infection. He developed extremely high serum bilirubin levels, probably attributed to the concomitant viral infection and his G6PD status. He recovered completely with conservative therapy. The present child is the youngest ever reported case till date with this complication secondary to HEV infection.
 ...
PMID:Acute pancreatitis--complicating hepatitis E virus infection in a 7-year-old boy with glucose 6 phosphate dehydrogenase deficiency. 1912 25

Hepatitis B virus (HBV) is a small DNA virus that targets the liver and infects humans worldwide. Recently we have shown that the metabolic regulator PGC-1alpha coactivates HBV transcription thereby rendering the virus susceptible to fluctuations in the nutritional status of the liver. PGC-1alpha coactivation of HBV is mediated through the liver-enriched nuclear receptor HNF4alpha and through another yet unknown transcription factor(s). Here we show that the forkhead transcription factor FOXO1, a known target for PGC-1alpha coactivation and a central mediator of glucose metabolism in the liver, binds HBV core promoter and activates its transcription. This activation is further enhanced in the presence of PGC-1alpha, implying that FOXO1 is a target for PGC-1alpha coactivation of HBV transcription. Thus, our results identify another key metabolic regulator as an activator of HBV transcription, thereby supporting the principle that HBV gene expression is regulated in a similar way to key hepatic metabolic genes.
 ...
PMID:The metabolic activator FOXO1 binds hepatitis B virus DNA and activates its transcription. 1923 23

A higher prevalence of glucose abnormalities has been reported in patients with hepatitis C virus (HCV) infection compared to patients with hepatitis B virus (HBV) infection. However, previous studies considered some confounding factors and ignored others, which might influence the comparative risk assessment between HBV and HCV infections. Fasting plasma glucose concentration, severity of liver disease and viral load were determined in 220 patients with HCV genotype 4 infection, and 200 patients with HBV infection. Patients completing antiviral therapy were followed-up, and the fasting plasma glucose levels were determined in patients with and without sustained virological response. The prevalence of glucose abnormalities in HCV infection (41%) was significantly higher than that in HBV infection (16%). However, when controlling the severity of liver disease and other risk factors, the prevalence of glucose abnormalities in patients with HCV infection was comparable to that in patients with HBV infection. After attaining of sustained virological response, a decrease of the median fasting plasma glucose value was observed only in chronic hepatitis C. In the group of patients with normal fasting plasma glucose levels, an association of nonsustained virological response with the development of impaired fasting glucose was only observed in chronic hepatitis C. The severity of liver disease was a common predictor of impaired fasting glucose in hepatitis B and C infections. These results indicate that high prevalence of glucose abnormalities can be associated with HBV- and HCV-related liver disease, and that clearance of HCV, but not HBV, may improve glucose metabolism.
 ...
PMID:Severity of liver disease predicts the development of glucose abnormalities in patients with chronic hepatitis B or C following achievement of sustained virological response to antiviral therapy. 1923 42

Hepatitis B virus, a member of the hepadnavirus family, causes the acute and chronic diseases of the human liver. The S domain of hepatitis B virus surface antigen (sHBsAg) was expressed under the control of the galactose-inducible GAL1 promoter in recombinant Saccharomyces cerevisiae. Batch fermentation of S. cerevisiae 2805/pdeltaMFalpha-sHBsAg resulted in 4.92gl(-1) dry cell mass and 2.21mgl(-1) sHBsAg concentration. To improve the expression level of sHBsAg, the pdi1 gene encoding protein disulfide isomerase was coexpressed in recombinant S. cerevisiae. Batch fermentation of S. cerevisiae 2805/pdeltaMFalpha-sHBsAg+pPDI using 21gl(-1) glucose and 33gl(-1) galactose resulted in 9.75gl(-1) dry cell mass and 13.3mgl(-1) sHBsAg concentration, which were 2 and 6 times higher than those for S. cerevisiae 2805/pdeltaMFalpha-sHBsAg, respectively. Appearance of three sHBsAgs with different molecular sizes of 24kDa, 34kDa and 40kDa in immunoblot assay and their endoglycosidase treatment indicated that sHBsAg might be expressed in three types of the authentic, MFalpha signal sequence-containing and N-glycosylated MFalpha signal sequence-containing forms. Fed-batch fermentation of recombinant S. cerevisiae 2805 coexpressing the sHBsAg and pdi1 genes was carried out by feeding 600gl(-1) glucose continuously and controlling galactose concentration at around 20gl(-1). As a result, 20.2gl(-1) dry cell mass and 74.4mgl(-1) maximum sHBsAg concentration were obtained, which were 4.1 and 33.7 times higher than those for the batch fermentation of S. cerevisiae 2805/pdeltaMFalpha-sHBsAg, respectively.
 ...
PMID:Expression of hepatitis B surface antigen S domain in recombinant Saccharomyces cerevisiae using GAL1 promoter. 1943 20

Most reported data on posttransplantation diabetes mellitus (PTDM) are from Western countries with patients who underwent deceased donor liver transplantation. A retrospective study was performed to assess the prevalence and predictive factors of PTDM in the context of living donor liver transplantation (LDLT) in the Chinese population using the definition of PTDM proposed in 2003 by the World Health Organization and the American Diabetes Association. The prevalence of DM after LDLT in our study was 25% (21/84), and the incidence of PTDM was 14.9% (11/74) with 64% of cases diagnosed within 3 months after LDLT; 9.5% were observed to show impaired fasting glucose postoperatively. Multivariate analysis identified body mass index >or= 25 kg/m(2) before LDLT as the only independent risk factor for developing PTDM. Only one patient was operated for hepatitis C virus (HCV) infection. Hepatitis B virus (HBV)-related diseases were common in our study population, accounting for 78.6% of all patients. Both HCV and HBV infection status were not independent risk factors for developing PTDM. In addition, a greater tacrolimus trough blood level in the PTDM group versus no-DM group was observed at 3 months post-LDLT (11.03 ng/mL vs 4.87 ng/mL). The mean tacrolimus dose was not significantly different between the two groups. In conclusion, PTDM was prevalent among Chinese LDLT recipients.
 ...
PMID:Diabetes mellitus after living donor liver transplantation: data from mainland China. 1954 22

Our previous work demonstrated that berberine (BBR) increases insulin receptor (InsR) expression and improves glucose utility both in vitro and in animal models. Here, we study the InsR-up-regulating and glucose-lowering activities of BBR in humans. Our results showed that BBR increased InsR messenger RNA and protein expression in a variety of human cell lines, including CEM, HCT-116, SW1990, HT1080, 293T, and hepatitis B virus-transfected human liver cells. Accordingly, insulin-stimulated phosphorylations of InsR beta-subunit and Akt were increased after BBR treatment in cultured cells. In the clinical study, BBR significantly lowered fasting blood glucose (FBG), hemoglobin A(1c), triglyceride, and insulin levels in patients with type 2 diabetes mellitus (T2DM). The FBG- and hemoglobin A(1c)-lowering efficacies of BBR were similar to those of metformin and rosiglitazone. In the BBR-treated patients, the percentages of peripheral blood lymphocytes that express InsR were significantly elevated after therapy. Berberine also lowered FBG effectively in chronic hepatitis B and hepatitis C patients with T2DM or impaired fasting glucose. Liver function was improved greatly in these patients by showing reduction of liver enzymes. Our results confirmed the activity of BBR on InsR in humans and its relationship with the glucose-lowering effect. Together with our previous report, we strongly suggest BBR as an ideal medicine for T2DM with a mechanism different from metformin and rosiglitazone.
 ...
PMID:Berberine lowers blood glucose in type 2 diabetes mellitus patients through increasing insulin receptor expression. 1980 84

The hepatitis B virus X-protein (HBx), a multifunctional viral regulator, participates in the viral life cycle and in the development of hepatocellular carcinoma (HCC). We previously reported a high incidence of HCC in transgenic mice expressing HBx. In this study, proteomic analysis was performed to identify proteins that may be involved in hepatocarcinogenesis and/or that could be utilized as early detection biomarkers for HCC. Proteins from the liver tissue of HBx-transgenic mice at early stages of carcinogenesis (dysplasia and hepatocellular adenoma) were separated by 2-DE, and quantitative changes were analyzed. A total of 22 spots displaying significant quantitative changes were identified using LC-MS/MS. In particular, several proteins involved in glucose and fatty acid metabolism, such as mitochondrial 3-ketoacyl-CoA thiolase, intestinal fatty acid-binding protein 2 and cytoplasmic malate dehydrogenase, were differentially expressed, implying that significant metabolic alterations occurred during the early stages of hepatocarcinogenesis. The results of this proteomic analysis provide insights into the mechanism of HBx-mediated hepatocarcinogenesis. Additionally, this study identifies possible therapeutic targets for HCC diagnosis and novel drug development for treatment of the disease.
 ...
PMID:Proteomic analysis of liver tissue from HBx-transgenic mice at early stages of hepatocarcinogenesis. 1981 10

Visfatin is a new adipokine involved in several processes. The data concerning visfatin in chronic hepatitis C (CHC) is small. To assess visfatin serum concentration and to study its association with biochemical and morphological features in CHC. Seventy nonobese patients with CHC (Group 1) confirmed by the presence of serum hepatitis C virus (HCV)-RNA and 20 healthy volunteers (Group 2), similar in age and BMI with normal fasting glucose and lipid profile were included. Visfatin was significantly increased in Group 1 compared with Group 2 (55.6 +/- 23.1 vs 23.7 +/- 3.8 ng/mL; P < 0.001). Visfatin was negatively associated with necro-inflammatory activity grade (r = -0.36; P = 0.007). The lowest levels were found in patients with the most advanced inflammation: grades 3-4 - 46.8 +/- 17.1, grade 2 - 52.6 +/- 18.4 and grade 1 - 75.2 +/- 27.6 ng/mL; P = 0.017. A significant difference was also shown comparing patients with minimal inflammatory activity to the rest of the cohort (P = 0.009). Visfatin receiver operating characteristic curve analysis for different necro-inflammatory activity - grade 1 vs grades 3-4 with area under the curve 0.81 indicated a good discriminant power for differentiation of moderate/severe inflammation, with the cut-off set at 57.6 ng/mL (sensitivity 75%, specificity 90%, positive predictive value 0.90, negative predictive value 0.75). Serum visfatin concentration increases significantly in CHC patients. These findings suggest that visfatin is important in the pathogenesis of the inflammatory process in CHC. Visfatin may play a dual role as a pro-inflammatory or/and protective factor. The measurement of visfatin serum concentration may serve as an additional tool in distinguishing more advanced grades of the necro-inflammatory activity.
 ...
PMID:Visfatin serum levels in chronic hepatitis C patients. 1984 Mar 67

Several studies have reported that obesity and diabetes are important risk factors for elevated blood aminotransferase activity in individuals with no underlying causes of liver disease. The aim of this study was to determine whether obesity and fasting glucose level were associated with hepatic dysfunction in patients with hepatitis B infection. A total of 934 patients with hepatitis B infection were enrolled, among whom increased alanine aminotransferase (ALT) activity (> or =40 IU/L) was observed in 25.1%. By univariate analysis, factors associated with increased ALT activity among patients with hepatitis B infection included body mass index (BMI), fasting blood glucose level, and blood triglyceride and high-density cholesterol levels. By multivariate logistic regression analysis, BMI and fasting blood glucose level were independent predictors of elevated ALT activity, with odds ratios of 1.73 (95% confidence interval, 1.17-2.56) for subjects with a BMI greater than or equal to 25 kg/m2 and 1.88 (95% confidence interval, 1.06-3.33) for subjects with a fasting blood glucose greater than or equal to 126 mg/dL. Even in subjects with ALT activity within the reference range, ALT activity was found to be associated with BMI. In conclusion, a BMI greater than or equal to 25 kg/m2 and a fasting blood glucose level greater than or equal to 126 mg/dL were risk factors for increased ALT activity in subjects with hepatitis B infection, suggesting that obesity and diabetic fasting hyperglycemia may aggravate liver injury in this population.
 ...
PMID:Obesity and diabetic hyperglycemia were associated with serum alanine aminotransferase activity in patients with hepatitis B infection. 1984 82

Recent studies have introduced serum uric acid (UA) as a potential risk factor for developing diabetes, hypertension, stroke, and cardiovascular diseases. The value of elevated levels of UA in serum as a risk factor for diabetes development is still under scrutiny. Recent data suggest that clearance of UA is being reduced with increase in insulin resistance and UA as a marker of prediabetes period. However, conflicting data related to UA in serum of patients with Type 2 diabetes prompted us to study the urine/serum ratio of UA levels (USRUA) in these patients and healthy controls. All subjects included in the study were free of evidence of hepatitis B or C viral infection or active liver and kidney damage. Patients receiving drugs known to influence UA levels were also excluded from this study. Analysis of glucose and uric acid were performed on Dade Behring analyzer using standard IFCC protocols. Interestingly, our data demonstrated about 2.5 fold higher USRUA values in diabetic patients as compared to control subjects. Furthermore, there was a trend of correlation of USRUA value with the blood glucose levels in diabetic patients, which was more prominent in diabetic men than in women. With aging, levels of uric acid increased in serum of diabetic patients, and this effect was also more profound in male than in female diabetics. In conclusion, this study showed significantly elevated USRUA levels in patients with Type 2 diabetes, a negative USRUA correlation with the blood glucose levels in diabetic patients, and an effect of sex and age on the uric acid levels. Since literature data suggest a strong genetic effect on UA levels, it would be pertinent to perform further, possibly genetic studies, in order to clarify gender and ethnic differences in UA concentrations.
 ...
PMID:Relevance of uric Acid in progression of type 2 diabetes mellitus. 2019 32


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>