Search results for "NAFL"

showing 10 items of 122 documents

Microparticles: Modulators and biomarkers of liver disease

2012

Division of Molecular and Translational Medicine,Dept. of Medicine I, Johannes Gutenberg University, Mainz, GermanyEmerging role of microparticlesMicroparticles (MP) have gained increasing attention as biomark-ers for various diseases. First described as platelet dust, MP wereregarded as unspecific debris [1]. However, it has become appar-ent that cell derived MP or ectosomes represent a novel route ofhorizontal communication between cells. MP are between 100–1000 nm in size and generated through cell membrane shedding(ectocytosis), a process that can be triggered by the activation ofthe complement C5b-9 complex, as shown for platelet derivedMP, or by inhibition of flippase activitythroughCa

Cell signalingCD14+MacrophageT cellCellApoptosisCell CommunicationBiologyMonocyteExosomeAnnexin VCD4+Cell membraneCell-Derived MicroparticlesmedicineHumansMacrophageEctosomeCD41+InflammationHepatologyLiver DiseasesMonocytePlateletNASHT cellBiomarkerDendritic cellCD8+FibrosisHepatitis CCell biologyExosomemedicine.anatomical_structureLiverMicroparticleBiochemistryNAFLiNKTBiomarkersDendritic cellJournal of Hepatology
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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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Genetic ablation of macrohistone H2A1 leads to increased leanness, glucose tolerance and energy expenditure in mice fed a high-fat diet.

2015

Contains fulltext : 155347.pdf (Publisher’s version ) (Closed access) BACKGROUND/OBJECTIVES: In the context of obesity, epigenetic mechanisms regulate cell-specific chromatin plasticity, perpetuating gene expression responses to nutrient excess. MacroH2A1, a variant of histone H2A, emerged as a key chromatin regulator sensing small nutrients during cell proliferation and differentiation. Mice genetically ablated for macroH2A1 (knockout (KO)) do not show overt phenotypes under a standard diet. Our objective was to analyse the in vivo role of macroH2A1 in response to nutritional excess. METHODS: Twelve-week-old whole-body macroH2A1 KO male mice were given a high-fat diet (60% energy from lard…

EXPRESSIONCHROMATINNonalcoholic steatohepatitisModels Molecularmedicine.medical_specialtyHISTONE VARIANT MACROH2Amacrohistone H2A1 High fat diet obesity.Endocrinology Diabetes and MetabolismLIVER-DISEASE NAFLDTHERMOGENESISMedicine (miscellaneous)Adipose tissueBiologyDiet High-FatCell LineHistonesMiceINFLAMMATIONAdipose Tissue BrownThinnessInternal medicineBINDINGmedicineAnimalsGenetic ablationNutrition and DieteticsAdipogenesisNONALCOHOLIC STEATOHEPATITISTRANSCRIPTIONAL COREGULATOR PELP1medicine.diseaseNUTRITION&DIETETICSObesityDisease Models AnimalRenal disorders Radboud Institute for Molecular Life Sciences [Radboudumc 11]EndocrinologyEnergy expenditureFat dietOBESITYInsulin ResistanceEnergy MetabolismThermogenesisInternational journal of obesity (2005)
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MAFLD: a multisystem disease

2023

Nonalcoholic fatty liver disease (NAFLD), affecting about 25% of general population and more than 50% of dysmetabolic patients, is an emerging cause of chronic liver disease and its complications. Recently, an international consensus of experts proposed to rename this disease as ‘Metabolic dysfunction-Associated Fatty Liver Disease’ (MAFLD) to focus on the bidirectional interplay between fatty liver and metabolic alterations and to stress the need of assessing fatty liver independently from alcohol consumption and other coexisting causes of liver disease. The peculiarity of NAFLD/MAFLD lies in the presence of a higher risk of not only – as expected – liver-related events but also of extrah…

Endocrinology Diabetes and Metabolismfatty liver MAFLD NAFLD
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Analisi molecolare di carcinomi epatocellulari istologicamente caratterizzati e correlazioni eziopatogenetiche

2023

Hepatocellular carcinoma NAFLD Molecular Pathology
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Macrophage MerTK promotes profibrogenic cross-talk with hepatic stellate cells via soluble mediators

2022

Background & aims: Activation of Kupffer cells and recruitment of monocytes are key events in fibrogenesis. These cells release soluble mediators which induce the activation of hepatic stellate cells (HSCs), the main fibrogenic cell type within the liver. Mer tyrosine kinase (MerTK) signaling regulates multiple processes in macrophages and has been implicated in the pathogenesis of non-alcoholic steatohepatitis-related fibrosis. In this study, we explored if MerTK activation in macrophages influences the profibrogenic phenotype of HSCs. Methods: Macrophages were derived from THP-1 cells or differentiated from peripheral blood monocytes towards MerTK+/CD206+/CD163+/CD209- macrophages. Th…

HepatologyCM conditioned medium ECM extracellular matrix Gas-6 Gas-6 growth arrest-specific gene 6 HSC(s) hepatic stellate cells KC(s) Kupffer cell(s) M-CSF macrophage colony-stimulating factor M2c-like macrophages MerTK Myeloid-epithelial-reproductive tyrosine kinase NAFLD non-alcoholic fatty liver disease NASH NASH non-alcoholic steatohepatitis PMA phorbol 12-myristate 13-acetate TGFβ1 transforming growth factor-β1 THP-1 TIMP1 tissue inhibitor of metalloproteinase 1 VEGF-A vascular endothelial growth factor-A liver fibrosis siRNA small-interfering RNAGas-6; liver fibrosis; M2c-like macrophages; NASH; THP-1GastroenterologyInternal MedicineImmunology and AllergyJHEP Reports
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AGILE 3+ Score for the Diagnosis of Advanced Fibrosis and for Predicting Liver-related Events in NAFLD.

2022

Background & aims: We aimed to assess the diagnostic accuracy of AGILE 3+, a recently developed score based on the combination of aspartate aminotransferase/alanine aminotransferase ratio, platelet count, diabetes status, sex, age, and liver stiffness measurement (LSM) by transient elastography, when compared with Fibrosis-4 (FIB-4) and LSM, for the diagnosis of advanced fibrosis and for the prediction of liver-related events (LREs) occurrence in patients with NAFLD. Methods: A total of 614 consecutive patients with biopsy-proven NAFLD or clinical diagnosis of NAFLD-related compensated cirrhosis were enrolled. LREs were recorded during follow-up. FIB-4, LSM by transient elastography (Fi…

HepatologyFibrosiNAFLDNASH.GastroenterologyAGILE 3+DCAClinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association
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Geographical similarity and differences in the burden and genetic predisposition of NAFLD

2022

: NAFLD has become a major public health problem for more than 2 decades with a growing prevalence in parallel with the epidemic of obesity and type 2 diabetes (T2D). The disease burden of NAFLD differs across geographical regions and ethnicities. Variations in prevalence of metabolic diseases, extent of urban-rural divide, dietary habits, lifestyles, and the prevalence of NAFLD risk and protective alleles can contribute to such differences. The rise in NAFLD has led to a remarkable increase in the number of cases of cirrhosis, hepatocellular carcinoma, hepatic decompensation, and liver-related mortality related to NAFLD. Moreover, NAFLD is associated with multiple extrahepatic manifestatio…

HepatologyNAFLD
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Noninvasive assessment of liver disease severity in patients with nonalcoholic fatty liver disease (NAFLD) and type 2 diabetes

2023

Background: We evaluated the diagnostic accuracy of simple non-invasive tests(NITs) in NAFLD patients with type 2 diabetes(T2D). Methods: This was an individual patient data meta-analysis of 1780 patients with biopsy-proven NAFLD and T2D. The index tests of interest were FIB-4, NAFLD Fibrosis Score(NFS), APRI, liver stiffness measurement(LSM) by vibration-controlled transient elastography(VCTE) and AGILE 3+. The target conditions were advanced fibrosis, nonalcoholic steatohepatitis(NASH) and fibrotic NASH(NASH plus F2-F4 fibrosis). The diagnostic performance of NITs individually or in sequential combination was assessed by area under receiver operating characteristic curve(AUROC) and by dec…

Hepatologynafld diabetes noninvasive fibrosis
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Metabolic Consequences of Obstructive Sleep Apnea

2022

The effects of OSA on metabolism are quite complex, and obesity, diabetes, nonalcoholic fatty liver disease and dyslipidemia often coexist with OSA, making it difficult to tease out the independent effects of OSA on metabolic variables. There is firm experimental evidence of a detrimental impact of OSA on adipose tissue dysfunction, with intermittent hypoxia, sympathetic hyperactivity, and oxidative stress as the most important intermediate mechanisms. Sleep fragmentation or deprivation may also contribute to the metabolic dysfunction of OSA. This work reviews the current knowledge on this topic, as well as the results of studies on the effects of CPAP treatment.

InflammationDiabetes mellitu...CholesterolFree fatty acidInsulin resistanceContinuous positive airway pressure (CPAP)Settore MED/10 - Malattie Dell'Apparato RespiratorioCardiovascular riskMetabolic syndromeNonalcoholic fatty liver disease (NAFLD)
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