Search results for "hepatocytes"

showing 4 items of 224 documents

Non-alcoholic fatty liver disease pathogenesis: The present and the future

2008

Non-alcoholic fatty liver disease is the clinical hepatic expression of metabolic syndrome. The prevalence of non-alcoholic fatty liver disease is around 20-30%, and with a rapid increase in the metabolic risk factors in the general population, non-alcoholic fatty liver disease has become the most common cause of liver disease worldwide. A fraction (20-30%) of non-alcoholic fatty liver disease patients develop a potentially progressive hepatic disorder, namely non-alcoholic steatohepatitis, leading to end-stage liver disease. The pathogenesis of non-alcoholic fatty liver disease is not entirely understood, and even if insulin resistance is a major pathogenetic key, many other factors are im…

medicine.medical_specialtyLipolysisPopulationPhysiologyApoptosisMitochondria LiverInsulin resistance Non-alcoholic fatty liver disease Non-alcoholic steatohepatitis SteatosisDiseaseFatty Acids NonesterifiedPathogenesisLiver diseaseInsulin resistanceAdipokinesRisk FactorsInternal medicinemedicineAnimalsHumansGenetic Predisposition to Diseaseeducationeducation.field_of_studyHepatologybusiness.industryFatty liverGastroenterologymedicine.diseaseDietFatty LiverOxidative StressEndocrinologyAdipose TissueLiverDisease ProgressionHepatocytesCytokinesInsulin ResistanceSteatohepatitisMetabolic syndromebusinessDigestive and Liver Disease
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Beta-2-glycoprotein I is growth regulated and plays a role as survival factor for hepatocytes

2004

Beta-2-glycoprotein I (beta(2)GPI) is mainly produced by the liver and is found in plasma partially associated to lipoproteins. Although various properties have been attributed to this protein, its physiological role remains still unclear. We investigated its expression in cultured liver cells and in regenerating liver. Expression studies in HepG2 cells demonstrate that beta(2)GPI mRNA is regulated in a cell cycle-dependent manner, with very low expression in low cycling conditions and increasing levels in proliferating cells. p21 WAF-dependent growth arrest, induced by butyrate treatment, down-regulate beta(2)GPI mRNA levels. Immunolocalization in normal rat liver shows a non-homogeneous p…

medicine.medical_specialtyRegenerating liverSurvivalCell SurvivalCell cycle expressionCellCell Culture TechniquesButyrateBiologyBiochemistrychemistry.chemical_compoundAlbuminsInternal medicineGene expressionmedicineAnimalsHumansBeta 2-Glycoprotein IRats WistarGlycoproteinsAlbuminSodium butyrateCell BiologyLiver RegenerationRatsBeta-2-glycoprotein ICell biologyButyratesEndocrinologymedicine.anatomical_structureGene Expression RegulationLiverchemistrybeta 2-Glycoprotein IHepatocytesApolipoprotein HHepatic stellate cellGDF15The International Journal of Biochemistry & Cell Biology
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A targeted apoB38.9 mutation in mice is associated with reduced hepatic cholesterol synthesis and enhanced lipid peroxidation.

2006

Familial hypobetalipoproteinemia (FHBL) due to truncation-specifying mutations of apolipoprotein B (apoB), which impair hepatic lipid export in very low-density lipoprotein (VLDL) particles, is associated with fatty liver. In an FHBL-like mouse with the apoB38.9 mutation, fatty liver develops despite reduced hepatic fatty acid synthesis. However, hepatic cholesterol contents in apoB38.9 mice are normal. We found that cholesterogenic enzymes (3-hydroxy-3-methylglutaryl-coenzyme A reductase, sterol-C5-desaturase, and 7-dehydrocholesterol reductase) were consistently downregulated in two separate expression-profiling experiments using a total of 19 mice ( n = 7 each for apob+/+and apob+/38.9, …

medicine.medical_specialtyVery low-density lipoproteinApolipoprotein BPhysiologymedicine.disease_causeLipid peroxidationHypobetalipoproteinemiaschemistry.chemical_compoundMicePhysiology (medical)Internal medicineNAFLDmedicineAnimalsFamilial hypobetalipoproteinemiamice modelCells CulturedApolipoproteins BMutationHepatologybiologyChemistryMutagenesisGastroenterologyGene targetingRatsFatty LiverMice Inbred C57BLEndocrinologyCholesterolLiverApolipoprotein B-100Gene Targetingbiology.proteinHepatocytesMutagenesis Site-Directedlipids (amino acids peptides and proteins)Lipid PeroxidationmutationOxidative stressLipoproteinAmerican journal of physiology. Gastrointestinal and liver physiology
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Antioxidant effect of melanoidins after induction of oxidative stress in isolated rat hepatocytes

2002

Se estudia el efecto de las melanoidinas en el estrés oxidativo inducido por adriamicina en hepatocitos aislados de rata. Las melanoidinas presentan un efecto protector, incrementando la viabilidad celular y protegiendo a los lípidos y a las proteínas del estrés oxidativo Melanoidins have a protective effect over macromolecules. They increase cellular viability and protect lipids and proteins from oxidative stress

melanoidinsUNESCO::CIENCIAS MÉDICASoxidative stresshepatocytes:CIENCIAS MÉDICAS [UNESCO]
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