Search results for "Nonalcoholic fatty liver"

showing 10 items of 142 documents

Retinol-binding protein 4: a new marker of virus-induced steatosis in patients infected with hepatitis C virus genotype 1.

2008

Retinol-binding protein 4 (RBP4) is an adipocytokine associated with insulin resistance (IR). We tested serum levels of RBP4 to assess its link with steatosis in patients with genotype 1 chronic hepatitis C (CHC) or nonalcoholic fatty liver disease (NAFLD). Nondiabetic patients with CHC (n = 143) or NAFLD (n = 37) were evaluated by liver biopsy and anthropometric and metabolic measurements, including IR by the homeostasis model assessment. Biopsies were scored by Scheuer classification for CHC, and Kleiner for NAFLD. Steatosis was tested as a continuous variable and graded as absent-mild <30%, or moderate-severe > or =30%. Thirty nondiabetic, nonobese blood donors served as controls. …

AdultMalemedicine.medical_specialtyGenotypeHepatitis C virusHepacivirusSettore MED/08 - Anatomia Patologicamedicine.disease_causeGastroenterologySeverity of Illness IndexInsulin resistanceRisk FactorsInternal medicineNonalcoholic fatty liver diseasemedicinesteatosisHumansRetinol-binding protein 4 .Retinol binding protein 4Settore MED/12 - GastroenterologiaHepatologybiologymedicine.diagnostic_testOdds ratioHepatologyHepatitis C ChronicMiddle Agedmedicine.diseaseFatty LiverLogistic ModelsLiverLiver biopsyImmunologybiology.proteinFemaleSteatosisRetinol-Binding Proteins PlasmaBiomarkers
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Low- and high-density lipoprotein subclasses in subjects with nonalcoholic fatty liver disease.

2014

BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is associated with increased cardiometabolic risk. Although dyslipidemia represents a key factor in this disease, its impact on serum levels of distinct lipoprotein subfractions is largely unknown.OBJECTIVE: To assess the full low-density lipoprotein (LDL) and high-density lipoprotein (I-EDL) profiles in patients with NAFLD.METHODS: Seven LDL and 10 HDL subfractions were assessed by gel electrophoresis (Lipoprint, Quantimetrix Corporation, USA) in men with biopsy proven NAFLD (simple steatosis [n = 17, age, 34 7 years] and nonalcoholic steatohepatitis [NASH; n = 24, age, 32 +/- 6 years]). Exclusion criteria included robust alcohol consump…

AdultMalemedicine.medical_specialtySimple steatosiEndocrinology Diabetes and MetabolismBody Mass Indexchemistry.chemical_compoundHigh-density lipoproteinInsulin resistanceNon-alcoholic Fatty Liver DiseaseRisk FactorsInternal medicineNonalcoholic fatty liver diseasemedicineInternal MedicineNutrition and DieteticNonalcoholic fatty liver diseaseHumansAspartate AminotransferasesLipoproteinNutrition and Dieteticsbiologybusiness.industryRisk FactorMedicine (all)Fatty livernutritional and metabolic diseasesAspartate AminotransferaseAlanine TransaminaseLipidMiddle Agedmedicine.diseaseAtherosclerosisFatty LiverLipoproteins LDLEndocrinologyAlanine transaminasechemistryAtherosclerosibiology.proteinFemaleNonalcoholic steatohepatitibusinessCardiology and Cardiovascular MedicineLipoproteins HDLBody mass indexDyslipidemiaLipoproteinHumanJournal of clinical lipidology
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Regulation of the effects of CYP2E1-induced oxidative stress by JNK signaling

2014

The generation of excessive amounts of reactive oxygen species (ROS) leads to cellular oxidative stress that underlies a variety of forms of hepatocyte injury and death including that from alcohol. Although ROS can induce cell damage through direct effects on cellular macromolecules, the injurious effects of ROS are mediated largely through changes in signal transduction pathways such as the mitogen-activated protein kinase c-Jun N-terminal kinase (JNK). In response to alcohol, hepatocytes have increased levels of the enzyme cytochrome P450 2E1 (CYP2E1) which generates an oxidant stress that promotes the development of alcoholic steatosis and liver injury. These effects are mediated in larg…

Alcoholic liver diseaseClinical BiochemistryReview ArticleMitogen-activated protein kinase kinasemedicine.disease_causeBiochemistryCytochrome P450 2E10302 clinical medicineMolecular Targeted TherapyMitogen-activated protein kinaseslcsh:QH301-705.5c-Jun N-terminal kinasechemistry.chemical_classificationTNF tumor necrosis factorlcsh:R5-9200303 health sciencesCell DeathCYP2E1 cytochrome P450 2E1Cytochrome P-450 CYP2E13. Good healthCell biologyPKD protein kinase DLiverJNK c-Jun N-terminal kinaseSab SH3 homology associated BTK binding protein030211 gastroenterology & hepatologySignal transductionlcsh:Medicine (General)MAP Kinase Signaling SystemAPAP acetaminophenMKK MAPK kinaseBiology03 medical and health sciencesROS reactive oxygen speciesPKC protein kinase CmedicineAnimalsHumansMAPKKK MAPK kinase kinaseProtein kinase ACell damage030304 developmental biologyReactive oxygen speciesMAP kinase kinase kinaseOrganic ChemistryJNK Mitogen-Activated Protein KinasesAlcoholic liver diseasemedicine.diseaseERK1/2 extracellular signal-regulated kinase 1/2Fatty Liverlcsh:Biology (General)chemistryOxidative stressNAFLD nonalcoholic fatty liver diseaseReactive Oxygen SpeciesMAPK mitogen-activated protein kinaseOxidative stressRedox Biology
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Including Ratio of Platelets to Liver Stiffness Improves Accuracy of Screening for Esophageal Varices That Require Treatment

2021

International audience; Background & aims: Based on platelets and liver stiffness measurements, the Baveno VI criteria (B6C), the expanded B6C (EB6C), and the ANTICIPATE score can be used to rule out varices needing treatment (VNT) in patients with compensated chronic liver disease. We aimed to improve these tests by including data on the ratio of platelets to liver stiffness.Methods: In a retrospective analysis of data from 10 study populations, collected from 2004 through 2018, we randomly assigned data from 2368 patients with chronic liver disease of different etiologies to a derivation population (n = 1579; 15.1% with VNT, 50.2% with viral hepatitis, 28.9% with nonalcoholic fatty liver …

Blood PlateletsLiver CirrhosisNoninvasive Diagnosismedicine.medical_specialtyCirrhosis[SDV]Life Sciences [q-bio]PopulationEsophageal and Gastric VaricesChronic liver diseaseSeverity of Illness IndexGastroenterologyEnd Stage Liver Disease03 medical and health sciencesLiver disease0302 clinical medicineModel for End-Stage Liver DiseaseEsophageal varicesInternal medicineNonalcoholic fatty liver diseasemedicineHumanseducationBaveno VI CriteriaRetrospective Studieseducation.field_of_studyHepatologybusiness.industryGastroenterologyRetrospective cohort studyPortal Hypertensionmedicine.disease3. Good healthMELDCirrhosis030220 oncology & carcinogenesisElasticity Imaging Techniques030211 gastroenterology & hepatologybusinessBaveno VI Criteria Blood Platelets Cirrhosis Elasticity Imaging Techniques End Stage Liver Disease Esophageal and Gastric Varices Humans Liver Cirrhosis MELD Noninvasive Diagnosis Portal Hypertension Retrospective Studies Severity of Illness Index
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Quercetin ameliorates dysregulation of lipid metabolism genes via the PI3K/AKT pathway in a diet-induced mouse model of nonalcoholic fatty liver dise…

2015

Scope Flavonoids and related compounds seem to have favorable effects on nonalcoholic fatty liver disease (NAFLD) progression, although the exact mechanisms implicated are poorly understood. In this study, we aimed to investigate the effect of the flanovol quercetin on gene expression deregulation involved in the development of NAFLD, as well as the possible implication of phosphatidylinositol 3-kinase (PI3K)/AKT pathway modulation. Methods and results We used an in vivo model based on methionine- and choline-deficient (MCD) diet-fed mice and an in vitro model consisting of Huh7 cells incubated with MCD medium. MCD-fed mice showed classical pathophysiological characteristics of nonalcoholic…

CD36 AntigensMalemedicine.medical_specialtyOxidative phosphorylationBiologyMicePhosphatidylinositol 3-Kinaseschemistry.chemical_compoundNon-alcoholic Fatty Liver DiseaseInternal medicineNonalcoholic fatty liver diseaseGene expressionmedicineTranscriptional regulationAnimalsLY294002PhosphatidylinositolCells CulturedPI3K/AKT/mTOR pathwayLipid metabolismLipid Metabolismmedicine.diseaseMice Inbred C57BLDisease Models AnimalOxidative StressEndocrinologyGene Expression RegulationchemistryCancer researchQuercetinLipid PeroxidationProto-Oncogene Proteins c-aktSignal TransductionFood ScienceBiotechnologyMolecular Nutrition & Food Research
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Nonalcoholic Fatty Liver Disease, Cardiovascular Risk, and Carotid Inflammation.

2015

Nonalcoholic fatty liver disease (NAFLD) is defined by excessive triglycerides (TGs) accumulation in the liver (>5% of hepatocytes histologically) in the absence of alcohol excess. The NAFLD ranges from simple steatosis to steatohepatitis and cirrhosis. The NAFLD and nonalcoholic steatohepatitis (NASH) are now the number one cause of liver disease in Western countries. The prevalence of NAFLD is increasing but is underreported, and the epidemiology and demographic characteristics vary worldwide. The prevalence is increasing because of the rising occurrence of obesity and type 2 diabetes (T2DM); in fact, NAFLD is considered as the hepatic manifestation of metabolic syndrome (MetS). Nonalcoho…

Carotid Artery Diseasesmedicine.medical_specialtyVery low-density lipoproteinLipoproteins//purl.org/becyt/ford/3.3 [https]Risk FactorsInternal medicineNonalcoholic fatty liver diseasemedicinePrevalenceHumansInflammationAdiponectinbusiness.industryFatty liverNon Alcoholic Fatty Liver Diseasenutritional and metabolic diseasesmedicine.diseasedigestive system diseasesFatty LiverOxidative StressEndocrinologyCardiovascular DiseasesDisease Progression//purl.org/becyt/ford/3 [https]Hepatic lipaseMetabolic syndromeSteatohepatitisInsulin ResistanceCardiology and Cardiovascular MedicinebusinessBiomarkersLipoproteinAngiology
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The Evolving Role of Fetuin-A in Nonalcoholic Fatty Liver Disease: An Overview from Liver to the Heart

2021

Nonalcoholic fatty liver disease (NAFLD) is strongly associated to the features of metabolic syndrome which can progress to cirrhosis, liver failure and hepatocellular carcinoma. However, the most common cause of mortality in people with NAFLD is not liver-related but stems from atherosclerotic cardiovascular disease (CVD). The prevalence of NAFLD is on the rise, mainly as a consequence of its close association with two major worldwide epidemics, obesity and type 2 diabetes (T2D). The exact pathogenesis of NAFLD and especially the mechanisms leading to disease progression and CVD have not been completely elucidated. Human fetuin-A (alpha-2-Heremans Schmid glycoprotein), a glycoprotein produ…

Cirrhosisalpha-2-HS-GlycoproteinQH301-705.5030209 endocrinology & metabolismReviewType 2 diabetes030204 cardiovascular system & hematologyBioinformaticsdigestive systemCatalysisInorganic ChemistryPathogenesis03 medical and health sciences0302 clinical medicineInsulin resistanceNon-alcoholic Fatty Liver DiseaseNAFLDNonalcoholic fatty liver diseaseAnimalsHumansMedicineBiology (General)Physical and Theoretical ChemistryQD1-999Molecular BiologyCVD Fetuin‐A NAFLD Animals Cardiovascular Diseases Fibrosis Humans Liver Non-alcoholic Fatty Liver Disease alpha-2-HS-GlycoproteinSpectroscopybusiness.industryOrganic Chemistrynutritional and metabolic diseasesGeneral MedicineCVDmedicine.diseaseFibrosisObesitydigestive system diseasesFetuin-AComputer Science ApplicationsChemistryLiverCardiovascular DiseasesHepatocellular carcinomaMetabolic syndromebusinessInternational Journal of Molecular Sciences
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Liver Fat, Adipose Tissue, and Body Composition Changes After Switching from a Protease Inhibitor or Efavirenz to Raltegravir.

2021

Integrase inhibitors appear to increase body weight, but paradoxically some data indicate that raltegravir (RAL) may decrease liver fat. Our objective was to study the effects of switching from a protease inhibitor (PI) or efavirenz (EFV) to RAL on liver fat, body composition, and metabolic parameters among people living with HIV (PLWH) with high risk for nonalcoholic fatty liver disease (NAFLD). We randomized overweight PLWH with signs of metabolic syndrome to switch a PI or EFV to RAL (

Cyclopropanesmedicine.medical_specialtyanimal structuresEfavirenzIntegrase inhibitorAdipose tissueHIV Infections03 medical and health scienceschemistry.chemical_compound0302 clinical medicineAdipocyteInternal medicineRaltegravir PotassiumNonalcoholic fatty liver diseasemedicineHumansProtease inhibitor (pharmacology)Protease Inhibitors030212 general & internal medicinebusiness.industryPublic Health Environmental and Occupational Healthmedicine.diseaseRaltegravir3. Good healthBenzoxazinesInfectious DiseasesEndocrinologychemistryAdipose TissueLiverAlkynesBody Composition030211 gastroenterology & hepatologymedicine.symptombusinessWeight gainmedicine.drugAIDS patient care and STDs
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Obesity and nonalcoholic fatty liver disease in type 1 diabetes mellitus patients

2022

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Diabetes Mellitus Type 1EndocrinologyNon-alcoholic Fatty Liver DiseaseEndocrinology Diabetes and MetabolismInternal MedicineHumansObesityCardiometabolic risk Diabetes mellitus type 1 Metabolic syndrome Nonalcoholic Nonalcoholic fatty liver disease Obesity SteatohepatitisJournal of Diabetes and its Complications
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Role of Myeloid-Epithelial-Reproductive Tyrosine Kinase and Macrophage Polarization in the Progression of Atherosclerotic Lesions Associated With Non…

2019

Recent lines of evidence highlight the involvement of myeloid-epithelial-reproductive tyrosine kinase (MerTK) in metabolic disease associated with liver damage. MerTK is mainly expressed in anti-inflammatory M2 macrophages where it mediates transcriptional changes including suppression of proinflammatory cytokines and enhancement of inflammatory repressors. MerTK is regulated by metabolic pathways through nuclear sensors including LXRs, PPARs, and RXRs, in response to apoptotic bodies or to other sources of cholesterol. Nonalcoholic fatty liver disease (NAFLD) is one of the most serious public health problems worldwide. It is a clinicopathological syndrome closely related to obesity, insuli…

Drug targeting0301 basic medicineMacrophageMacrophage polarizationInflammationReviewMonocyteProinflammatory cytokine03 medical and health sciencesMerTK0302 clinical medicineFibrosisNonalcoholic fatty liver diseasemedicineNonalcoholic fatty liver diseaseMacrophagePharmacology (medical)InflammationPharmacologybusiness.industrylcsh:RM1-950Lipid metabolismMERTKmedicine.diseasemacrophagesAtherosclerosis; Drug targeting; Inflammation; Macrophages; MerTK; Monocytes; Nonalcoholic fatty liver diseaselcsh:Therapeutics. Pharmacology030104 developmental biologyAtherosclerosi030220 oncology & carcinogenesisCancer researchatherosclerosismedicine.symptommonocytesbusinessFrontiers in Pharmacology
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