Upregulated hepatic expression of mitochondrial PEPCK triggers initial gluconeogenic reactions in the HCV-3 patients
Autor: | Taimoor I. Sheikh, Tashfeen Adam, Ishtiaq Qadri |
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Rok vydání: | 2015 |
Předmět: |
Medicine(all)
Hepatic steatosis G6PC medicine.medical_specialty Hepatitis C virus Diabetes Metabolic disorder HCV genotype 3 FOXO1 General Medicine Biology medicine.disease medicine.disease_cause Fold change Reverse transcription polymerase chain reaction Mitochondrial PEPCK Endocrinology Hyperglycemia Internal medicine Diabetes mellitus medicine Glucose homeostasis |
Zdroj: | Asian Pacific Journal of Tropical Medicine. 8:618-623 |
ISSN: | 1995-7645 |
DOI: | 10.1016/j.apjtm.2015.07.016 |
Popis: | Objective To identify the differential expression of candidate gluconeogenic genes which may initiate hepatitis C virus (HCV) related metabolic disorder during early stages of disease. Methods Patients of diverse age and sex, with positive HCV genotype 3 (HCV-3) RNA in serum and with no history of other related infections, co-infections, alcoholism, diabetes or chemotherapeutic treatments were considered for this study. Semi-quantitative reverse transcriptase PCR analysis and quantitative fold change analysis of the fresh liver biopsies of eight chronically infected HCV-3 patients and six healthy individuals were evaluated for three potential biomarkers involved in glucose homeostasis induction, namely mitochondrial phosphoenolpyruvate carboxykinase 2 (PCK2), glucose-6-phosphatase catalytic subunit (G6PC) and associated forkhead box protein 01 (FOXO1). Results Symptomatic evaluation, clinical history and blood test were conducted according to general disease prognosis procedures and reported here. Significantly upregulated expression of PCK2 independent of age, sex and viral infectivity levels in all HCV patients was observed, whereas no significant changes in the expression of G6PC and FOXO1 were found. Conclusions PCK2 triggers initial gluconeogenic reactions which ultimately result in the accumulation of glycogen in the liver hepatocytes. We therefore suggest that the overproduction of PCK2 has important physiological role in the onset of metabolic disorder in the HCV-3 patients. |
Databáze: | OpenAIRE |
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