Search results for "Insulin"

showing 10 items of 1360 documents

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
researchProduct

Haem oxygenase-1 regulates catabolic and anabolic processes in osteoarthritic chondrocytes

2007

Pro-inflammatory cytokines, matrix metalloproteinases (MMPs) and other catabolic factors participate in the pathogenesis of cartilage damage in osteoarthritis (OA). Pro-inflammatory cytokines such as interleukin-1β (IL-1β) mediate cartilage degradation and might be involved in the progression of OA. Previously, we found that haem oxygenase-1 (HO-1) is down-regulated by pro-inflammatory cytokines and up-regulated by IL-10 in OA chondrocytes. The aim of this study was to determine whether HO-1 can modify the catabolic effects of IL-1β in OA cartilage and chondrocytes. Up-regulation of HO-1 by cobalt protoporphyrin IX significantly reduced glycosaminoglycan degradation elicited by IL-1β in OA …

Cartilage ArticularMaleMAP Kinase Signaling Systemmedicine.medical_treatmentInterleukin-1betaProtoporphyrinsMatrix metalloproteinaseChondrocytePathology and Forensic MedicineExtracellular matrixChondrocytesmedicineExtracellularHumansInsulin-Like Growth Factor ICollagen Type IICells CulturedAggrecanAgedbiologyChemistryCartilageGrowth factorOsteoarthritis KneeMatrix MetalloproteinasesCell biologymedicine.anatomical_structureProteoglycanImmunologybiology.proteinFemaleProteoglycansHeme Oxygenase-1The Journal of Pathology
researchProduct

Insulin-like growth factors counteract the effect of interleukin 1 beta on type II phospholipase A2 expression and arachidonic acid release by rabbit…

1994

International audience; Interleukin 1 beta was found to stimulate arachidonic acid release, and the synthesis and secretion of type II phospholipase A2 by rabbit articular chondrocytes in vitro. Interleukin 1 beta had no effect on the level of cytosolic phospholipase A2 mRNA. Insulin-like growth factors, which help stabilize the cartilage matrix, reduced the effect of interleukin 1 beta on type II phospholipase A2 activity and mRNA level, and decreased the Interleukin 1 beta-stimulated arachidonic acid release to the basal values. This suggests that type II phospholipase A2 plays a key role in arachidonic acid release from rabbit articular chondrocytes and that insulin-like growth factors c…

Cartilage Articularmedicine.medical_specialtymedicine.medical_treatmentBiophysicsIn Vitro TechniquesBiochemistryChondrocytePhospholipases AInterleukin 1βInsulin-like growth factorchemistry.chemical_compoundPhospholipase A2[ CHIM.ORGA ] Chemical Sciences/Organic chemistryPhospholipase A2Structural BiologyInsulin-Like Growth Factor IIInternal medicineGeneticsmedicineAnimalsInsulin-like growth factorRNA MessengerInsulin-Like Growth Factor IMolecular BiologyArachidonic Acidbiology[CHIM.ORGA]Chemical Sciences/Organic chemistryArthritisInterleukinCell Biology[CHIM.ORGA] Chemical Sciences/Organic chemistryChondrocyteSomatomedinPhospholipases A2Endocrinologymedicine.anatomical_structureCytokinechemistryInsulin-like growth factor 2biology.proteinArachidonic acidRabbitsInterleukin-1
researchProduct

Dynamics of Ca2+ and guanosine 5'-[gamma-thio]triphosphate action on insulin secretion from alpha-toxin-permeabilized HIT-T15 cells.

1994

The time course of Ca2+ and GTP-analogue effects on insulin secretion was investigated in HIT-T15 cells permeabilized with Staphylococcus alpha-toxin. These cells responded to Ca2+ in the range 0.1-10 microM and could be used in a dynamic perifusion system because of the minimal run-down of the secretory response. High Ca2+ (10 microM) elicited a monophasic ATP-dependent stimulation of insulin secretion that reached a peak within 5 min (approximately 20-fold increase) and rapidly decreased during the subsequent 15 min to a plateau remaining above basal rates (0.1 microM Ca2+). The decrease in Ca(2+)-induced insulin secretion with time could not be attributed to decreased capacity to respond…

Cell Membrane PermeabilityGTP'medicine.medical_treatmentStimulationCalcium-Calmodulin-Dependent Protein Kinases - antagonists & inhibitorsBiochemistryPiperazinesAdenosine TriphosphateDesensitization (telecommunications)1-(5-Isoquinolinesulfonyl)-2-MethylpiperazineInsulin SecretionGuanosine 5'-O-(3-Thiotriphosphate) - pharmacologyStaphylococcus aureus alpha-toxinInsulinGuanosine Triphosphate - pharmacologyGuanylyl ImidodiphosphateKinasePiperazines - pharmacologyInsulin secretionAdenosine Triphosphate - pharmacologyPermeabilized cellsGuanosine TriphosphateResearch Articlemedicine.medical_specialtyStaphylococcus aureuschemistry.chemical_elementBiologyCalciumGuanylyl Imidodiphosphate - pharmacologyExocytosisCell LineInsulin - secretionInternal medicinemedicine1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - analogs & derivativesSecretionMolecular BiologyInsulinCell BiologyIsoquinolinesATPKineticsEndocrinologyCalcium - pharmacologychemistryIsoquinolines - pharmacologyGuanosine 5'-O-(3-Thiotriphosphate)Type C PhospholipasesCalcium-Calmodulin-Dependent Protein KinasesCalciumType C Phospholipases - pharmacologyGTP
researchProduct

Soluble N-ethylmaleimide-sensitive-factor attachment protein and N-ethylmaleimide-insensitive factors are required for Ca2+-stimulated exocytosis of …

1996

Ca2+ stimulates exocytosis in permeabilized insulin-secreting cells. To investigate the putative cytosolic components involved in the Ca2+ response, HIT-T15 cells (a pancreatic B-cell line) were permeabilized with streptolysin-O, a procedure that allows rapid exchange of soluble components including macromolecules. We found that in this cell preparation the secretory response to Ca2+ but not to guanosine 5'-[gamma-thio]triphosphate was lost as a function of time and could be restored by rat brain cytosol in a concentration-dependent manner. Reconstitutive activity of rat brain cytosol was found in a high-molecular-mass heat-labile partially N-ethylmaleimide(NEM)-sensitive fraction. The NEM-…

Cell Membrane Permeabilitymedicine.medical_treatmentBlotting WesternVesicular Transport ProteinsGuanosineBiologyBiochemistryExocytosisExocytosislaw.inventionCell Linechemistry.chemical_compoundIslets of LangerhansCytosolBacterial ProteinslawInsulin SecretionmedicineAnimalsInsulinheterocyclic compoundsAttachment proteinMolecular BiologyN-Ethylmaleimide-Sensitive ProteinsBrain ChemistryInsulinN-EthylmaleimideMembrane ProteinsCell BiologyRecombinant ProteinsCell biologyRatsSoluble N-Ethylmaleimide-Sensitive Factor Attachment ProteinsCytosolchemistryEthylmaleimideGuanosine 5'-O-(3-Thiotriphosphate)StreptolysinsRecombinant DNACalciumSoluble NSF attachment proteinCarrier ProteinsResearch ArticleThe Biochemical journal
researchProduct

Synthesis of insulin and its effects in Y79 human retinoblastoma cells

1994

This paper demonstrates that Y79 human retinoblastoma cells contain immunoreactive insulin (IRI) and release it in the medium. Cells cultured either in suspension or in monolayer showed a similar content of IRI. Moreover, in both conditions, IRI concentration was higher in cells cultured in serum-supplemented medium rather than in serum-free medium. Retinoblastoma cells are capable of synthesizing insulin. This was demonstrated by incubating Y79 cells with [3H]leucine. The synthesized radioactive insulin was separated and assayed by means of a HPLC procedure described in this paper. Both cell growth and [3H]thymidine and [3H]uridine incorporation into acid-insoluble fraction was reduced (-7…

Cell divisionmedicine.medical_treatmentBiologyCellular and Molecular Neurosciencechemistry.chemical_compoundLeucinemedicineTumor Cells CulturedHumansInsulinRNA NeoplasmCycloheximideInsulin-Like Growth Factor IChromatography High Pressure LiquidCell growthInsulinGrowth factorEye NeoplasmsRetinoblastomaDNA Neoplasmretinoblastoma cellsSensory SystemsUridineIn vitroOphthalmologychemistryBiochemistryCell cultureThymidineCell Division
researchProduct

In vivo reprogramming for tissue repair.

2015

Berninger and colleagues define milestones for in vivo reprogramming and discuss recent developments in reprogramming into pancreatic b-cells and neurons. Vital organs such as the pancreas and the brain lack the capacity for effective regeneration. To overcome this limitation, an emerging strategy consists of converting resident tissue-specific cells into the cell types that are lost due to disease by a process called in vivo lineage reprogramming. Here we discuss recent breakthroughs in regenerating pancreatic β-cells and neurons from various cell types, and highlight fundamental challenges that need to be overcome for the translation of in vivo lineage reprogramming into therapy.

Cell typeLineage (genetic)Cell- and Tissue-Based TherapyAcinar CellsBiologyIn vivoInsulin-Secreting CellsmedicineHumansRegenerationCell LineagePancreasNeuronsBrain DiseasesRegeneration (biology)BrainPancreatic DiseasesTranslation (biology)Cell DifferentiationCell BiologyTissue repairCellular ReprogrammingCell biologymedicine.anatomical_structurePancreasReprogrammingNeurogliaNature cell biology
researchProduct

The Role of the Heme Oxygenase System in the Metabolic Syndrome

2014

Molecular chaperones and the heat shock response play a major role in the maintenance of cellular homeostasis under various pathological conditions. In particular, their role is to regulate protein conformation, protect proteins from misfolding and aggregation, and maintain signalling and organellarnetworks. Among variousheat shock proteins, Hsp32 also known as heme oxygenase-1 (HO-1), has demonstrated an important role in metabolic syndrome. In particular, the HO system seems to play a major role in the complex pathophysiological cascade involved in insulin resistance mechanisms, and adipocyte functions as measured by the release of important adipokynes. The aim of the present review is to…

Cellular homeostasisBiologychemistry.chemical_compoundProtein structureInsulin resistanceDrug DiscoverymedicineHumansMetabolic syndrome heme oxygenase insulin sensitivity adiponectin heat shock proteins.Heat shockHemeHeat-Shock ProteinsMetabolic SyndromePharmacologySettore BIO/16 - Anatomia Umanamedicine.diseaseCell biologyHeme oxygenasechemistryBiochemistryShock (circulatory)Insulin Resistancemedicine.symptomMetabolic syndromeHeme Oxygenase-1Molecular Chaperones
researchProduct

Destruction of Kupffer’s cells increases total liver blood flow and decreases ischemia reperfusion injury in pigs

2000

Cellular immunityPathologymedicine.medical_specialtyAdenosineCell SurvivalKupffer CellsSwineAllopurinolmedicine.medical_treatmentOrgan Preservation SolutionsIschemiaHemodynamicsGadoliniumVena Cava InferiorHepatic ArteryRaffinoseAnimalsInsulinMedicineTransplantationChemotherapyPortal Veinbusiness.industryAnastomosis SurgicalKupffer cellOrgan PreservationBlood flowmedicine.diseaseGlutathioneLiver TransplantationTransplantationmedicine.anatomical_structureLiverRegional Blood FlowReperfusion InjuryImmunologySurgerybusinessReperfusion injuryLiver CirculationTransplantation Proceedings
researchProduct

Can Alzheimer disease be a form of type 3 diabetes?

2012

Alzheimer disease (AD) and metabolic syndrome are two highly prevalent pathological conditions of Western society due to incorrect diet, lifestyle, and vascular risk factors. Recent data have suggested metabolic syndrome as an independent risk factor for AD and pre-AD syndrome. Furthermore, biological plausibility for this relationship has been framed within the “metabolic cognitive syndrome” concept. Due to the increasing aging of populations, prevalence of AD in Western industrialized countries will rise in the near future. Thus, new knowledge in the area of molecular biology and epigenetics will probably help to make an early molecular diagnosis of dementia. An association between metabo…

Central Nervous SystemAgingmedicine.medical_specialtySingle-nucleotide polymorphismType 2 diabetesBiologyBioinformaticsPolymorphism Single NucleotideSHIP2 ADAlzheimer DiseaseRisk FactorsDiabetes mellitusInternal medicinemedicineDiabetes MellitusDementiaHumansInsulinEpigeneticsRisk factorLife StyleAgedSettore MED/04 - Patologia GeneraleMetabolic SyndromeInositol Polyphosphate 5-PhosphatasesSyndromeModels Theoreticalmedicine.diseasePhosphoric Monoester HydrolasesEndocrinologySettore MED/26 - NeurologiaGeriatrics and GerontologyAlzheimer's diseaseMetabolic syndromeCognition DisordersSignal TransductionRejuvenation research
researchProduct