Search results for " liver disease"

showing 10 items of 559 documents

Niemann-Pick type C2 protein supplementation in experimental non-alcoholic fatty liver disease

2017

BACKGROUND AND AIMS: Hepatic cholesterol deposition drives inflammation and fibrosis in non-alcoholic steatohepatitis (NASH). The Niemann-Pick type C2 (NPC2) protein plays an important role in regulating intracellular cholesterol trafficking and homeostasis. We hypothesized that intravenous NPC2 supplementation reduces cholesterol accumulation, hepatic inflammation and fibrogenesis in a nutritional NASH rat model.METHODS: Rats were fed a high-fat, high-cholesterol (HFHC) diet for four weeks resulting in moderately severe NASH. Animals were treated with intravenous NPC2 or placebo twice weekly for either the last two weeks or the entire four weeks. End-points were liver/body- and spleen/body…

0301 basic medicinePhysiologyGene Expressionlcsh:MedicinePathology and Laboratory MedicineBiochemistrychemistry.chemical_compound0302 clinical medicineNon-alcoholic Fatty Liver DiseaseFibrosisImmune PhysiologyMedicine and Health Scienceslcsh:ScienceImmune ResponseSterol Regulatory Element Binding ProteinsInnate Immune SystemMultidisciplinarybiologyLiver DiseasesReverse cholesterol transportFatty liverIntracellular Signaling Peptides and ProteinsLipidsCholesterolLiverCytokinesLiver FibrosisFemale030211 gastroenterology & hepatologylipids (amino acids peptides and proteins)Research Articlemedicine.medical_specialtyImmunologyBiological Transport ActiveGastroenterology and HepatologyCollagen Type I03 medical and health sciencesSigns and SymptomsDiagnostic MedicineInternal medicineGeneticsmedicineAnimalsRats WistarGlycoproteinsNutritionInflammationbusiness.industryCholesterollcsh:RBiology and Life Sciencesnutritional and metabolic diseasesMolecular Developmentmedicine.diseaseDietary FatsFibrosisRatsDietCollagen Type I alpha 1 ChainPPAR gammaFatty LiverDisease Models Animal030104 developmental biologyEndocrinologychemistryImmune SystemABCA1LDL receptorbiology.proteinlcsh:QSteatohepatitisCarrier ProteinsbusinessDevelopmental BiologyLipoprotein
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Nutritional Intake and the Risk for Non-Alcoholic Fatty Liver Disease (NAFLD)

2019

The prevalence of non-alcoholic fatty liver disease (NAFLD) is rising worldwide, and it is estimated that approximately one billion individuals may be afflicted with NAFLD globally [...]

0301 basic medicinePhysiologylcsh:TX341-641DiseaseGlobal Healthdigestive system03 medical and health sciences0302 clinical medicineFeeding behaviorNon-alcoholic Fatty Liver DiseaseGlobal healthMedicineHumans030109 nutrition & dieteticsNutrition and Dieteticsbusiness.industryFatty livernutritional and metabolic diseasesNon alcoholicFeeding BehaviorDietary patternmedicine.diseasedigestive system diseasesEditorialn/a030211 gastroenterology & hepatologybusinesslcsh:Nutrition. Foods and food supplyFood ScienceNutrients
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Kinase-independent functions of RIPK1 regulate hepatocyte survival and liver carcinogenesis.

2017

The mechanisms that regulate cell death and inflammation play an important role in liver disease and cancer. Receptor-interacting protein kinase 1 (RIPK1) induces apoptosis and necroptosis via kinase-dependent mechanisms and exhibits kinase-independent prosurvival and proinflammatory functions. Here, we have used genetic mouse models to study the role of RIPK1 in liver homeostasis, injury, and cancer. While ablating either RIPK1 or RelA in liver parenchymal cells (LPCs) did not cause spontaneous liver pathology, mice with combined deficiency of RIPK1 and RelA in LPCs showed increased hepatocyte apoptosis and developed spontaneous chronic liver disease and cancer that were independent of TNF…

0301 basic medicineProgrammed cell deathLiver tumorCell SurvivalNecroptosisMice TransgenicBiologyChronic liver diseaseProinflammatory cytokine03 medical and health sciencesLiver diseaseMiceLiver Neoplasms ExperimentalmedicineAnimalsDiethylnitrosamineKinase activityTranscription Factor RelAGeneral Medicinemedicine.disease3. Good healthNeoplasm Proteins030104 developmental biologymedicine.anatomical_structureCell Transformation NeoplasticReceptors Tumor Necrosis Factor Type IHepatocyteReceptor-Interacting Protein Serine-Threonine KinasesCancer researchHepatocytesSignal TransductionResearch ArticleThe Journal of clinical investigation
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Outcome of liver transplantation for hepatopulmonary syndrome: a Eurotransplant experience.

2019

Hepatopulmonary syndrome (HPS) is a pulmonary vascular complication of liver disease that affects up to 30% of patients with cirrhosis [1]. Intrapulmonary vascular dilatations and shunts result in gas exchange abnormalities, ranging from elevated alveolar-arterial oxygen gradients with no hypoxemia to very severe hypoxemia [1, 2]. Currently, liver transplantation (LT) is the only treatment option [3]. The Model for End-Stage Liver Disease (MELD) is a scoring system for assessing liver disease severity that has been validated to predict the 3-months waitlist mortality, and is used by Eurotransplant for prioritising allocation of liver transplants [4]. Footnotes This manuscript has recently b…

0301 basic medicinePulmonary and Respiratory MedicineRiskScoring systemmedicine.medical_treatmentMedizinVascular complicationLiver transplantationEnd Stage Liver Disease03 medical and health sciences0302 clinical medicineSevere hypoxemiaNothingMedicineHumansRegistriesProportional Hazards ModelsRetrospective Studiesbusiness.industryConflict of interestTreatment optionsLiver TransplantationEuropeOxygen030104 developmental biologyTreatment OutcomeLaw030211 gastroenterology & hepatologybusinessProduction teamHepatopulmonary SyndromeThe European respiratory journal
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Impact of PNPLA3 and IFNL3 polymorphisms on hepatic steatosis in Asian patients with chronic hepatitis C.

2017

Background and aims A recent meta-analysis revealed that the genotype PNPLA3 rs738409 GG is associated with a higher risk of hepatic steatosis (HS) in Caucasian patients with chronic hepatitis C (CHC). However, controversial results were found regarding Asian populations. Furthermore, previous studies have shown a negative association between interferon lambda 3 (IFNL3) rs12979860 CC and HS in Caucasian CHC patients, but there have been no reports indicating any such association in Asian populations. In this study, then, we investigated the association of PNPLA3 and IFNL3 polymorphisms with HS in Asian CHC patients. Methods We enrolled consecutive CHC patients who underwent liver biopsy pri…

0301 basic medicineRNA virusesMaleSteatosisHeredityPhysiologylcsh:MedicineHepacivirusChronic liver diseasePathology and Laboratory MedicineGastroenterologyBody Mass IndexCytopathologyLiver disease0302 clinical medicineEndocrinologyGenotypeMedicine and Health Scienceslcsh:ScienceMultidisciplinaryAlcohol Consumptionmedicine.diagnostic_testHepatitis C virusFatty liverHepatitis CMedical microbiologyMiddle AgedGenetic MappingPhysiological ParametersLiverLiver biopsyViruses030211 gastroenterology & hepatologyFemalePathogensResearch ArticleAdultmedicine.medical_specialtyEndocrine DisordersVariant GenotypesMicrobiologyPolymorphism Single Nucleotide03 medical and health sciencesAsian PeopleInternal medicinemedicineGeneticsDiabetes MellitusHumansGenetic Predisposition to DiseaseAllelesGenetic Association StudiesNutritionAgedFlavivirusesbusiness.industryInterleukinsBody Weightlcsh:ROrganismsViral pathogensBiology and Life SciencesMembrane ProteinsLipaseHepatitis C Chronicmedicine.diseaseFibrosisHepatitis virusesDietMicrobial pathogensFatty Liver030104 developmental biologyAnatomical PathologyGenetic LociMetabolic Disorderslcsh:QInterferonsSteatosisbusinessBody mass indexDevelopmental BiologyPLoS ONE
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Altilix® Supplement Containing Chlorogenic Acid and Luteolin Improved Hepatic and Cardiometabolic Parameters in Subjects with Metabolic Syndrome: A 6…

2019

The objective was to evaluate the effects of 6 months of supplementation with Altilix&reg

0301 basic medicineSettore MED/09 - Medicina Internacynaragenetic structuresPlacebo-controlled study030204 cardiovascular system & hematologySettore BIO/09 - FisiologiaGastroenterology0302 clinical medicineDiabetes mellitusimmune system diseasescardiovascular diseasehemic and lymphatic diseasesBrachial arteryLuteolinNutrition and Dieteticsdiabetes mellituFatty liverhemic and immune systemsDietary supplementsMetabolic syndromeCardiovascular diseasesLivertype 2diabetes mellitusChlorogenic Acidlcsh:Nutrition. Foods and food supplymedicine.medical_specialtyWaistlcsh:TX341-641chemical and pharmacologic phenomenaCynaraPlacebometabolic syndromedietary supplements03 medical and health sciencesDouble-Blind MethodInternal medicineDiabetes mellitusmedicine.arterymedicinebusiness.industrynon-alcoholic fatty liver diseasemedicine.diseasecardiovascular diseases030104 developmental biologydietary supplementSteatosisMetabolic syndromebusinessFood ScienceNon-alcoholic fatty liver disease
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GSK-3 in liver diseases: Friend or foe?

2020

Liver diseases, including hepatitis due to hepatitis B or C virus infection, non-alcoholic fatty liver disease, and hepatocellular carcinoma pose major challenges for overall health due to limited curative treatment options. Thus, there is an urgent need to develop new therapeutic strategies for the treatment of these diseases. A better understanding of the signaling pathways involved in the pathogenesis of liver diseases can help to improve the efficacy of emerging therapies, mainly based on pharmacological approaches, which influence one or more specific molecules involved in key signal transduction pathways. These emerging therapies are very promising for the prevention and treatment of …

0301 basic medicineSignaling pathwaysDruggabilityDiseaseBioinformaticsNon-alcoholic fatty liver disease (NAFLD)Glycogen Synthase Kinase 303 medical and health sciences0302 clinical medicineGSK-3Glycogen synthase kinase 3 (GSK-3)AnimalsHumansMedicineHepatitis B virus (HBV)Molecular Targeted TherapyEnzyme InhibitorsHepatocellular carcinoma (HCC)Molecular BiologyHepatitisbusiness.industryLiver DiseasesFatty liverDisease ManagementHepatitis C virus (HCV)Cell BiologyHepatitis Bmedicine.disease030104 developmental biologyGene Expression RegulationMultigene Family030220 oncology & carcinogenesisHepatocellular carcinomaHost-Pathogen InteractionsDisease SusceptibilitySignal transductionbusinessBiomarkersSignal TransductionBiochimica et Biophysica Acta (BBA) - Molecular Cell Research
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Fasting inhibits hepatic stellate cells activation and potentiates anti-cancer activity of Sorafenib in hepatocellular cancer cells

2017

BACKGROUND: Hepatocellular carcinoma (HCC) has a poor outcome. Most HCCs develop in the context of liver fibrosis and cirrhosis caused by chronic inflammation. Short-term fasting approaches enhance the activity of chemotherapy in preclinical cancer models, other than HCC. Multi-tyrosine kinase inhibitor Sorafenib is the mainstay of treatment in HCC. However, its benefit is frequently short-lived. Whether fasting can alleviate liver fibrosis and whether combining fasting with Sorafenib is beneficial remains unknown. METHODS: 24 hour fasting (2% serum, 0.1% glucose)-induced changes on human hepatic stellate cells (HSC) LX-2 proliferation/viability/cell cycle were assessed by MTT and flow cyto…

0301 basic medicineSorafenibLipopolysaccharidesNiacinamidemedicine.medical_specialtyCirrhosisCarcinoma HepatocellularTime FactorsPhysiologyGlucose uptakeClinical BiochemistryAntineoplastic AgentsLiver Cirrhosis Experimental03 medical and health sciencesFibrosisNon-alcoholic Fatty Liver DiseaseInternal medicineSorafenib fastingmedicineHepatic Stellate CellsAnimalsHumansneoplasmsCell Proliferationhepatic stellate cellDose-Response Relationship Drugbusiness.industryMedicine (all)Phenylurea CompoundsLiver NeoplasmsCancerCell BiologyFastingHep G2 Cellshepatocellular carcinomaSorafenibmedicine.diseasedigestive system diseasesGene Expression Regulation NeoplasticMice Inbred C57BL030104 developmental biologyEndocrinologyGlucoseHepatocellular carcinomaHepatic stellate cellCancer researchSteatohepatitisbusinessmedicine.drug
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Insulin resistance and hyperandrogenism drive steatosis and fibrosis risk in young females with PCOS

2017

Background and aims Nonalcoholic fatty liver disease (NAFLD) and polycystic ovary syndrome (PCOS) recognize obesity and insulin resistance (IR) as common pathogenic background. We assessed 1) whether PCOS is a risk factor for steatosis, and 2) the impact, in PCOS patients, of IR and hyperandrogenism on steatosis and fibrosis. Methods We considered 202 consecutive Italian PCOS nondiabetic patients and 101 age-matched controls. PCOS was diagnosed applying the Rotterdam diagnostic criteria. Steatosis was diagnosed if hepatic steatosis index (HSI) >36, while fibrosis by using the FIB-4 score. As surrogate estimate of insulin sensitivity we considered the insulin sensitivity index (ISI). Free an…

0301 basic medicineSteatosisendocrine system diseasesPhysiologylcsh:MedicinePathology and Laboratory MedicineBiochemistryBody Mass IndexCytopathology0302 clinical medicineEndocrinologyNon-alcoholic Fatty Liver DiseaseRisk FactorsNonalcoholic fatty liver diseaseMedicine and Health SciencesInsulinlcsh:ScienceMultidisciplinaryLiver DiseasesFatty liverMiddle AgedPolycystic ovaryLipidsCholesterolOncologyPhysiological Parameters030211 gastroenterology & hepatologyFemalePolycystic Ovary SyndromeResearch ArticleAdultmedicine.medical_specialtyGastroenterology and Hepatology03 medical and health sciencesInsulin resistanceInternal medicinemedicineHumansObesityRisk factorTriglyceridesDiabetic Endocrinologybusiness.industryFree androgen indexHyperandrogenismCholesterol HDLBody Weightlcsh:RCancers and NeoplasmsBiology and Life Sciencesmedicine.diseaseFibrosisHormonesFatty Liver030104 developmental biologyEndocrinologyAnatomical Pathologylcsh:QSteatosisInsulin ResistancebusinessHyperandrogenismGynecological TumorsDevelopmental Biologyinsulin resistance PCOS
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Junctional adhesion molecules JAM-B and JAM-C promote autoimmune-mediated liver fibrosis in mice

2018

Fibrosis remains a serious health concern in patients with chronic liver disease. We recently reported that chemically induced chronic murine liver injury triggers increased expression of junctional adhesion molecules (JAMs) JAM-B and JAM-C by endothelial cells and de novo synthesis of JAM-C by hepatic stellate cells (HSCs). Here, we demonstrate that biopsies of patients suffering from primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC) or autoimmune hepatitis (AIH) display elevated levels of JAM-C on portal fibroblasts (PFs), HSCs, endothelial cells and cholangiocytes, whereas smooth muscle cells expressed JAM-C constitutively. Therefore, localization and function of JA…

0301 basic medicine[SDV]Life Sciences [q-bio]Cholangitis SclerosingMyocytes Smooth MuscleeducationImmunologyImmunoglobulinsAutoimmune hepatitisVascular RemodelingChronic liver diseaseMural cellPrimary sclerosing cholangitisFatty Acids MonounsaturatedMice03 medical and health sciencesFibrosisCell AdhesionmedicineAnimalsHumansImmunology and AllergyMyofibroblastsCells CulturedInflammationMice KnockoutFibrous capsule of GlissonLiver Cirrhosis Biliarybusiness.industryfungiEndothelial Cellsmedicine.diseaseFibrosishumanities3. Good healthMice Inbred C57BLDisease Models AnimalHepatitis Autoimmune030104 developmental biologyLiverVasoconstrictioncardiovascular systemCancer researchHepatic stellate cellFemaleHepatic fibrosisbusinessCell Adhesion MoleculesJournal of Autoimmunity
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