Search results for "steatohepatitis"

showing 10 items of 134 documents

Prevalence and determinants of non-alcoholic fatty liver disease in lifelines: A large Dutch population cohort

2017

BACKGROUND & AIMS Non-alcoholic fatty liver disease is an increasing health issue that develops rather unnoticed with obesity, type 2 diabetes mellitus and metabolic syndrome. We investigated prevalence, determinants and associated metabolic abnormalities of non-alcoholic fatty liver disease in the largest population-based cohort to date. METHODS Biochemical characteristics, type 2 diabetes mellitus and metabolic syndrome were determined in the Lifelines Cohort Study (N = 167,729), a population-based cohort in the North of the Netherlands. Non-alcoholic fatty liver disease was defined as Fatty Liver Index (FLI)≥60. Exclusion criteria were age <18 years, immigrants, missing data to assess FL…

0301 basic medicineMaleCirrhosislcsh:MedicineGastroenterologyBiochemistryGLOMERULAR-FILTRATION-RATESTEATOHEPATITISWhite Blood Cells0302 clinical medicineEndocrinologyNon-alcoholic Fatty Liver DiseaseRisk FactorsAnimal CellsPrevalenceMedicine and Health SciencesDiabetes diagnosis and managementlcsh:ScienceNetherlandsMETABOLIC SYNDROME2. Zero hungerINSULIN-RESISTANCEMultidisciplinaryLiver DiseasesFatty liverMiddle AgedLipids3. Good healthType 2 DiabetesCholesterolHypertension030211 gastroenterology & hepatologyFemaleAnatomyCellular TypesResearch ArticleAdultmedicine.medical_specialtyHbA1cEndocrine DisordersImmune CellsImmunologyUNITED-STATESGastroenterology and Hepatology03 medical and health sciencesInsulin resistanceInternal medicineDiabetes mellitusmedicineDiabetes MellitusHumansHemoglobinHEPATIC STEATOSISHepatitisBlood Cellsbusiness.industryCholesterol HDLlcsh:RType 2 Diabetes MellitusBiology and Life SciencesProteinsRenal SystemCell Biologymedicine.diseaseDiagnostic medicineFatty LiverSERUM CREATININE VALUESRENAL-DISEASE030104 developmental biologyEndocrinologyCross-Sectional StudiesDiabetes Mellitus Type 2ATHEROSCLEROSISHyperglycemiaMetabolic DisordersRISK-FACTORSlcsh:QSteatohepatitisMetabolic syndromebusiness
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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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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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Impaired Kupffer Cell Self-Renewal Alters the Liver Response to Lipid Overload during Non-alcoholic Steatohepatitis

2020

International audience; Kupffer cells (KCs) are liver-resident macrophages that self-renew by proliferation in the adult independently from monocytes. However, how they are maintained during non-alcoholic steatohepatitis (NASH) remains ill defined. We found that a fraction of KCs derived from Ly-6C+ monocytes during NASH, underlying impaired KC self-renewal. Monocyte-derived KCs (MoKCs) gradually seeded the KC pool as disease progressed in a response to embryo-derived KC (EmKC) death. Those MoKCs were partly immature and exhibited a pro-inflammatory status compared to EmKCs. Yet, they engrafted the KC pool for the long term as they remained following disease regression while acquiring matur…

0301 basic medicine[SDV]Life Sciences [q-bio]OntogenyMESH: Cell Self RenewalSelf renewalMESH: MonocytesMESH: Mice KnockoutMice0302 clinical medicineNon-alcoholic Fatty Liver DiseaseImmunology and AllergyKupffer cellsMESH: AnimalsCell Self RenewalMESH: Lipid MetabolismMice KnockoutKupffer cellLipidsResearch Highlightmacrophages[SDV] Life Sciences [q-bio]Infectious Diseasesmedicine.anatomical_structureLiver030220 oncology & carcinogenesismonocytesmedicine.medical_specialtynon-alcoholic steatohepatitis (NASH)ImmunologyBiology03 medical and health sciencesMESH: Mice Inbred C57BLMESH: Cell ProliferationInternal medicinemedicineAnimalsLiver damageMESH: MiceCell ProliferationMESH: Non-alcoholic Fatty Liver DiseaseTriglyceride storageNon alcoholicLipid Metabolismmedicine.diseaseMESH: Lipidseye diseasesMice Inbred C57BLMESH: Kupffer Cells030104 developmental biologyEndocrinologySteatohepatitisHomeostasisMESH: LiverImmunity
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Hepatic B cell leukemia-3 promotes hepatic steatosis and inflammation through insulin-sensitive metabolic transcription factors.

2016

Background & Aims The pathomechanisms underlying non-alcoholic fatty liver disease (NAFLD) and the involved molecular regulators are incompletely explored. The nuclear factor-kappa B (NF-κB)-cofactor gene B cell leukemia-3 ( Bcl-3 ) plays a critical role in altering the transcriptional capacity of NF-κB – a key inducer of inflammation – but also of genes involved in cellular energy metabolism. Methods To define the role of Bcl-3 in non-alcoholic steatohepatitis (NASH), we developed a novel transgenic mouse model with hepatocyte-specific overexpression of Bcl-3 ( Bcl-3 Hep ) and employed a high-fat, high-carbohydrate dietary feeding model. To characterize the transgenic model, deep RNA seque…

0301 basic medicinemedicine.medical_specialtyCirrhosisCarcinoma Hepatocellularmedicine.medical_treatmentBiology03 medical and health sciencesLiver diseaseMice0302 clinical medicineB-Cell Lymphoma 3 ProteinInternal medicineProto-Oncogene ProteinsmedicineAnimalsHumansInsulinInflammationHepatologyInsulinLiver cellFatty liverLiver Neoplasmsmedicine.disease030104 developmental biologyEndocrinology030220 oncology & carcinogenesisLipogenesisSteatohepatitisSteatosisTranscription FactorsJournal of hepatology
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NUPR1 protects liver from lipotoxic injury by improving the endoplasmic reticulum stress response

2021

AbstractBackground and AimsNon-alcoholic fatty liver disease and related hepatic syndromes affect up to one third of the adult population. The molecular mechanisms underlying NAFL etiology remain elusive. Nuclear Protein 1 (NUPR1) expression increases upon cell injury in all organs and recently we report its active participation in the activation of the Unfolded Protein Response (UPR). The UPR typically maintains protein homeostasis, but downstream mediators of the pathway regulate metabolic functions, including lipid metabolism. NUPR1 and UPR increase have been reported in obesity and liver pathologies and the goal of this study was to investigate the roles of NUPR1 in this context.Methods…

0301 basic medicinemedicine.medical_specialtySettore MED/09 - Medicina InternaPPAR-a signalling UPRPeroxisome proliferator-activated receptorContext (language use)UPRDiet High-FatBiochemistry03 medical and health sciencesLiver diseaseMice0302 clinical medicineInternal medicineCell Line TumorGeneticsmedicineBasic Helix-Loop-Helix Transcription FactorsAnimalsHomeostasisHumansMolecular Biologychemistry.chemical_classificationbusiness.industryEndoplasmic reticulumFatty liverNASHLipid metabolismlipotoxicitymedicine.diseaseEndoplasmic Reticulum StressLipid MetabolismNeoplasm Proteins030104 developmental biologyEndocrinologychemistryLipotoxicityLiverNAFLKnockout mouseUnfolded protein responseUnfolded Protein ResponsePPAR-a signallingSteatosisSteatohepatitisbusiness030217 neurology & neurosurgeryNUPR1Biotechnology
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Beyond the Paradigm of Weight Loss in Non-Alcoholic Fatty Liver Disease: From Pathophysiology to Novel Dietary Approaches

2021

Current treatment recommendations for non-alcoholic fatty liver disease (NAFLD) rely heavily on lifestyle interventions. The Mediterranean diet and physical activity, aiming at weight loss, have shown good results in achieving an improvement of this liver disease. However, concerns related to compliance and food accessibility limit the feasibility of this approach, and data on the long-term effects on liver-related outcomes are lacking. Insulin resistance is a central aspect in the pathophysiology of NAFLD; therefore, interventions aiming at the improvement of insulin sensitivity may be preferable. In this literature review, we provide a comprehensive summary of the available evidence on nu…

0301 basic medicinemedicine.medical_specialtyinsulinlifestyletime-restricted feedingsteatohepatitisDiseaseReviewmetabolic syndrome03 medical and health sciencesLiver disease0302 clinical medicineInsulin resistanceNon-alcoholic Fatty Liver DiseaseWeight lossIntermittent fastingmedicineTime‐restricted feedingHumansTX341-641Intensive care medicineLife StyleNutrition and DieteticsNon‐alcoholicbusiness.industryNutrition. Foods and food supplyintermittent fastinglow-carb dietFatty liverfibrosismedicine.diseaseDietGastrointestinal MicrobiomeLow‐carb diet030104 developmental biologynon-alcoholicFibrosis; Insulin; Intermittent fasting; Lifestyle; Liver disease; Low‐carb diet; Metabolic syndrome; Non‐alcoholic; Steatohepatitis; Time‐restricted feeding; Weight loss030211 gastroenterology & hepatologyInsulin ResistanceSteatohepatitismedicine.symptomMetabolic syndromeweight lossbusinessliver diseaseFood ScienceNutrients
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2020

Understanding the importance of the gut microbiota (GM) in non-alcoholic fatty liver disease (NAFLD) has raised the hope for therapeutic microbes. We have shown that high hepatic fat content associated with low abundance of Faecalibacterium prausnitzii in humans and, further, the administration of F. prausnitzii prevented NAFLD in mice. Here, we aimed at targeting F. prausnitzii by prebiotic xylo-oligosaccharides (XOS) to treat NAFLD. First, the effect of XOS on F. prausnitzii growth was assessed in vitro. Then, XOS was supplemented or not with high (HFD, 60% of energy from fat) or low (LFD) fat diet for 12 weeks in Wistar rats (n = 10/group). XOS increased F. prausnitzii growth, having onl…

0301 basic medicinemedicine.medical_specialtymedicine.medical_treatmentFaecalibacterium prausnitziiButyrateGut floradigestive system03 medical and health sciences0302 clinical medicineInternal medicinemedicinechemistry.chemical_classificationNutrition and DieteticsbiologyPrebioticFatty liverfood and beveragesnutritional and metabolic diseasesFatty acidmedicine.diseasebiology.organism_classification3. Good health030104 developmental biologyEndocrinologychemistry030211 gastroenterology & hepatologySteatosisSteatohepatitisFood ScienceNutrients
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Steatohepatitis Impairs T-cell-Directed Immunotherapies Against Liver Tumors in Mice.

2019

Background & Aims Nonalcoholic steatohepatitis causes loss of hepatic CD4+ T cells and promotes tumor growth. The liver is the most common site of distant metastases from a variety of malignancies, many of which respond to immunotherapy. We investigated the effects of steatohepatitis on the efficacy of immunotherapeutic agents against liver tumors in mice. Methods Steatohepatitis was induced by feeding C57BL/6NCrl or BALB/c AnNCr mice a methionine and choline–deficient diet or a choline-deficient l-amino acid–defined diet. Mice were given intrahepatic or subcutaneous injections of B16 melanoma and CT26 colon cancer cells, followed by intravenous injections of M30-RNA vaccine (M30) or intrap…

0301 basic medicinemedicine.medical_treatmentT cellT-LymphocytesArticleMetastasis03 medical and health sciencesMice0302 clinical medicineImmune systemNon-alcoholic Fatty Liver DiseaseNonalcoholic fatty liver diseasemedicineAnimalsMelanomaTumor microenvironmentMice Inbred BALB CHepatologybiologybusiness.industryLiver NeoplasmsGastroenterologyImmunotherapymedicine.diseaseMice Inbred C57BLDisease Models Animal030104 developmental biologymedicine.anatomical_structurebiology.proteinCancer research030211 gastroenterology & hepatologyImmunotherapySteatohepatitisAntibodybusinessGastroenterology
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&lt;i&gt;NR1H4&lt;/i&gt; rs35724 G&amp;gt;C Variant Modulates Liver Damage in Nonalcoholic Fatty Liver Disease

2020

Background and Aims: Farnesoid X receptor (FXR) plays a key role in bile acid and lipid homeostasis. Experimental evidence suggests that it can modulate liver damage related to nonalcoholic fatty liver disease (NAFLD). We examined the impact of the NR1H4 rs35724 variant, encoding for FXR, on liver damage in a large cohort of patients at risk of steatohepatitis. Methods: We considered 2,660 consecutive individuals at risk of steatohepatitis with liver histology. The rs35724 G>C polymorphisms was genotyped by TaqMan assays. Gene expression was evaluated by RNASeq in a subset of patients (n=124). Results: The NR1H4 rs35724 variant was protective against severity of steatosis (OR 0.89, 95% C.I.…

0303 health sciencesmedicine.medical_specialtyBile acidCholesterolbusiness.industrymedicine.drug_class030302 biochemistry & molecular biologymedicine.diseaseGastroenterology3. Good health03 medical and health scienceschemistry.chemical_compoundchemistryFibrosisInternal medicineNonalcoholic fatty liver diseasemedicineCYP39A1Farnesoid X receptorSteatosisSteatohepatitisbusiness030304 developmental biologySSRN Electronic Journal
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