Search results for "Insulin"

showing 10 items of 1360 documents

Demonstration of an endocrine signaling circuit for insulin in the sponge Geodia cydonium.

1989

Abstract The existence of an insulin-mediated cell-to-cell signaling in the sponge Geodia cydonium is demonstrated in this study by molecular biological and immunological techniques. The sequence of a sponge cDNA clone encoding preproinsulin was analyzed for the first time and determined to comprise a high homology to human preproinsulin (60-80% homology). The predicted polypeptide of preproinsulin from sponge contains two disulfide bridges which link the A- to the B-chain. The intra-A chain disulfide bridge is absent. Applying immunological and electron microscopical techniques it is shown that insulin is produced in specialized cells (spherulous cells). Experimental evidence is presented …

PreproinsulinAnnexinsCellular differentiationBlotting WesternMolecular Sequence DataBiologyGeneral Biochemistry Genetics and Molecular BiologySequence Homology Nucleic AcidAnimalsHumansInsulinAmino Acid SequenceProtein PrecursorsReceptorMolecular BiologyPancreatic hormoneProinsulinGeneral Immunology and MicrobiologyBase SequenceGeneral NeuroscienceCalcium-Binding ProteinsDNAImmunohistochemistryReceptor InsulinPoriferaMicroscopy ElectronBiochemistryGene Expression RegulationHormone receptorSignal transductionHormoneResearch ArticleProinsulinSignal Transduction
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PIK3R1 Mutations Cause Syndromic Insulin Resistance with Lipoatrophy

2013

International audience; Short stature, hyperextensibility of joints and/or inguinal hernia, ocular depression, Rieger anomaly, and teething delay (SHORT) syndrome is a developmental disorder with an unknown genetic cause and hallmarks that include insulin resistance and lack of subcutaneous fat. We ascertained two unrelated individuals with SHORT syndrome, hypothesized that the observed phenotype was most likely due to de novo mutations in the same gene, and performed whole-exome sequencing in the two probands and their unaffected parents. We then confirmed our initial observations in four other subjects with SHORT syndrome from three families, as well as 14 unrelated subjects presenting wi…

ProbandEXPRESSIONmedicine.medical_specialty030209 endocrinology & metabolismBiologymedicine.disease_causeMICE LACKINGShort stature03 medical and health sciencesHYPOGLYCEMIA0302 clinical medicineInsulin resistancePIK3R1Internal medicineReportmedicineGeneticsKINASEGenetics(clinical)LipoatrophyGenetics (clinical)030304 developmental biology0303 health sciencesMutationAKT2[SDV.GEN]Life Sciences [q-bio]/GeneticsRECEPTORmedicine.disease3-KINASE3. Good healthInsulin receptorEndocrinologyAUTOPHOSPHORYLATIONSHORT syndromebiology.proteinSKELETAL-MUSCLEGROWTHmedicine.symptom[ SDV.GEN ] Life Sciences [q-bio]/Genetics
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Insulin and IGFs induce apoptosis in chick embryo retinas deprived of L-glutamine

1999

In chick embryo retinas, cultured in serum-free medium lacking L-glutamine, IGF-I, IGF-II and insulin induced apoptotic DNA fragmentation and cell death, IGF-I being the most efficacious compound. The apoptotic effect, which was particularly evident in retinas removed from 7-day-old chick embryos, declined with the age of the embryos and disappeared after day 11. Apoptosis appeared after a time lag of 8 h and then increased with time up to 16 h. Cycloheximide, an inhibitor of protein synthesis, was capable of entirely abolishing apoptotic cell death. The effect induced by IGFs or insulin was suppressed by the addition of glutamine. Cytokine-mediated apoptosis was also observed after withdra…

Programmed cell deathChemistryInsulinmedicine.medical_treatmentApoptotic DNA fragmentationEmbryoRetinalCell BiologyAnatomyCycloheximideCell biologyGlutaminechemistry.chemical_compoundApoptosismedicineInsulin apoptosis chick embryo retina development growth factorsMolecular Biology
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Processing without proteolytic cleavage is required for recognition of insulin by T cells.

1990

Beef insulin as well as a chymotryptic A-chain fragment [BI-A1-14(SSO3-)3] need uptake by antigen-presenting cells (APC) for efficient presentation in combination with major histocompatibility complex class II molecules to insulin-specific T cells. This could be shown by the inability of aldehyde-fixed APC to present these antigens to T cells. Furthermore, presentation of the insulin fragment as well as presentation of ovalbumin (OVA) was inhibited by treatment of APC with chloroquine, cerulenin or tunicamycin. This was not the case for a processing-independent OVA peptide. Treatment of APC during antigen pulsing with various protease inhibitors, active on all classes of proteases, did not …

ProteasesOvalbuminmedicine.medical_treatmentT-LymphocytesImmunologyAntigen presentationAntigen-Presenting CellsBiologyIn Vitro TechniquesEpitopeCell Linechemistry.chemical_compoundMiceAntigenEndopeptidasesmedicineImmunology and AllergyAnimalsInsulinProtease InhibitorsAntigen-presenting cellProteaseInsulinTunicamycinChloroquineTunicamycinEndocytosischemistryBiochemistryEuropean journal of immunology
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Processing requirements for the recognition of insulin fragments by murine T cells.

1988

In this study we investigated aspects of antigen processing using insulin and insulin A chain-derived fragments as model antigens in Ab alpha Ak beta-restricted T-cell stimulation. Similarly to other proteins, the immunodominant region of insulin recognized by these T cells is limited in size. It is located on the insulin A chain and encompasses a portion of the molecule that is represented faithfully by peptide A1-14(SSO3-)3. Efficient presentation of intact insulin and its entire A chain is dependent on uptake and processing by APC. Whereas peptides stemming from various globular proteins are known to be presented to T cells by APC without requiring processing, this is not the case with A…

Protein Denaturationmedicine.medical_treatmentT-LymphocytesImmunologyReceptors Antigen T-CellAntigen-Presenting CellsPeptideLymphocyte ActivationMajor Histocompatibility Complexchemistry.chemical_compoundEpitopesAntigenmedicineImmunology and AllergyAnimalsInsulinchemistry.chemical_classificationMHC class IIbiologyAntigen processingInsulinT-cell receptorTunicamycinClone CellsRatsBiochemistrychemistrybiology.proteinInsulin processingImmunological reviews
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Proteomic and transcriptomic profiling reveals a link between the PI3K pathway and lower estrogen-receptor (ER) levels and activity in ER+ breast can…

2010

Introduction Accumulating evidence suggests that both levels and activity of the estrogen receptor (ER) and the progesterone receptor (PR) are dramatically influenced by growth-factor receptor (GFR) signaling pathways, and that this crosstalk is a major determinant of both breast cancer progression and response to therapy. The phosphatidylinositol 3-kinase (PI3K) pathway, a key mediator of GFR signaling, is one of the most altered pathways in breast cancer. We thus examined whether deregulated PI3K signaling in luminal ER+ breast tumors is associated with ER level and activity and intrinsic molecular subtype. Methods We defined two independent molecular signatures of the PI3K pathway: a pro…

ProteomeMessengerEstrogen receptorPhosphatidylinositol 3-Kinases0302 clinical medicineReceptorsTumor Cells CulturedInsulin-Like Growth Factor IReceptorCancerOligonucleotide Array Sequence AnalysisMedicine(all)0303 health sciencesCulturedTumorBlottingReverse Transcriptase Polymerase Chain ReactionPrognosis3. Good healthTumor CellsGene Expression Regulation NeoplasticReceptors Estrogen030220 oncology & carcinogenesisFemaleSignal transductionWesternmedicine.drugBiotechnologySignal TransductionResearch Articlemedicine.medical_specialtyBlotting WesternOncology and CarcinogenesisBreast NeoplasmsBiology03 medical and health sciencesInternal medicineProgesterone receptorBreast CancerBiomarkers TumormedicineGeneticsHumansRNA MessengerOncology & CarcinogenesisPI3K/AKT/mTOR pathway030304 developmental biologyCell ProliferationNeoplasticCell growthGene Expression ProfilingEstrogenGene expression profilingEndocrinologyGene Expression RegulationCancer researchRNAProto-Oncogene Proteins c-aktTamoxifenBiomarkersBreast Cancer Research : BCR
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In Vitro Phenotypic, Genomic and Proteomic Characterization of a Cytokine-Resistant Murine β-TC3 Cell Line

2012

Type 1 diabetes mellitus (T1DM) is caused by the selective destruction of insulin-producing β-cells. This process is mediated by cells of the immune system through release of nitric oxide, free radicals and pro-inflammatory cytokines, which induce a complex network of intracellular signalling cascades, eventually affecting the expression of genes involved in β-cell survival. The aim of our study was to investigate possible mechanisms of resistance to cytokine-induced β-cell death. To this purpose, we created a cytokine-resistant β-cell line (β-TC3R) by chronically treating the β-TC3 murine insulinoma cell line with IL-1β + IFN-γ. β-TC3R cells exhibited higher proliferation rate and resistan…

ProteomicsAnatomy and Physiologymedicine.medical_treatmentCell Culture Techniqueslcsh:MedicineApoptosisSettore MED/13 - EndocrinologiaMiceEndocrinologyImmune PhysiologyInsulin-Secreting CellsMolecular Cell BiologySOCS3lcsh:ScienceMultidisciplinaryCell DeathDiabetes mellitus cytokines. apoptosis SUMO4 NF-kBCell CycleNF-kappa BGenomicsCell cycleImmunohistochemistryCell biologyPhenotypeCytokineMedicineCytokinesResearch ArticleProgrammed cell deathCell SurvivalImmunologyDown-RegulationBiologyAutoimmune DiseasesCell LineDownregulation and upregulationmedicineAnimalsGene SilencingBiologyCell ProliferationDiabetic EndocrinologyEndocrine PhysiologyCell growthlcsh:RCell cultureApoptosisImmune SystemClinical ImmunologyInsulinomalcsh:QPLoS ONE
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The role of gut micorbiome in obesity and diabetes

2019

Background Obesity and diabetes became a grooving problem in both adults and children. Many hypotheses concerned agents involved in the excessive weight gain process and it’s consequences. Not only genetic or environmental factors, but also intestinal microbiome seems to play a role in the pathophysiology of this phenomenon. Data sources A systematic review was conducted using Pubmed as the medical database source. Studies concerning connection between microbiome and metabolic disorders such as obesity and diabetes from last 10 years were analyzed. Results Intestinal bacteria may be involved both in the development of obesity, and its further complications. The pro-infammatory and immunomod…

Psychological interventionBioinformaticslaw.invention03 medical and health sciencesProbiotic0302 clinical medicineInsulin resistancelaw030225 pediatricsDiabetes mellitusDiabetes MellitusMedicineHumans030212 general & internal medicineMicrobiomeObesityHost Microbial Interactionsbusiness.industryDiabetesmedicine.diseaseObesityGastrointestinal MicrobiomePediatrics Perinatology and Child HealthCarbohydrate Metabolism DisorderDysbiosisDisease SusceptibilityMicrobiomebusinessDysbiosisWorld Journal of Pediatrics
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Metabolic syndrome, insulin resistance and sleepiness in real-life obstructive sleep apnoea.

2011

The metabolic syndrome shows a variable prevalence in obstructive sleep apnoea (OSA), and its association with insulin resistance or excessive daytime sleepiness in OSA is unclear. This study assessed the following in consecutive patients with newly diagnosed OSA: 1) the prevalence of metabolic syndrome; and 2) its association with insulin resistance and daytime sleepiness. Metabolic syndrome (National Cholesterol Education Program Adult Treatment Panel (NCEP- ATP) III criteria), insulin resistance (Homeostatic Model Assessment (HOMA) index, n5288) and daytime sleepiness (Epworth Sleepiness Scale) were assessed in 529 OSA patients. The prevalence of metabolic syndrome was 51.2%, which incre…

Pulmonary and Respiratory MedicineAdultMalemedicine.medical_specialtyExcessive daytime sleepinessBlood PressureSettore MED/10 - Malattie Dell'Apparato RespiratorioSeverity of Illness IndexBody Mass IndexInsulin resistanceSex FactorsInternal medicinemedicinePrevalenceHumansObesityAgedMetabolic SyndromeSleep Apnea Obstructivebusiness.industryEpworth Sleepiness ScaleSleep apneaMiddle Agedmedicine.diseaseObesityrespiratory tract diseasesOxygenEndocrinologyEpidemiology intermittent hypoxia metabolism sexHomeostatic model assessmentCardiologyFemaleSleep StagesMetabolic syndromemedicine.symptomInsulin ResistancebusinessBody mass indexBiomarkersThe European respiratory journal
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Sleep, sleep-disordered breathing and metabolic consequences.

2009

Sleep profoundly affects metabolic pathways. In healthy subjects, experimental sleep restriction caused insulin resistance (IR) and increased evening cortisol and sympathetic activation. Increased obesity in subjects reporting short sleep duration leads to speculation that, during recent decades, decreased sleeping time in the general population may have contributed to the increasing prevalence of obesity. Causal inference is difficult due to lack of control for confounders and inconsistent evidence of temporal sequence. In the general population, obstructive sleep apnoea (OSA) is associated with glucose intolerance. OSA severity is also associated with the degree of IR. However, OSA at bas…

Pulmonary and Respiratory MedicineAdultMalemedicine.medical_specialtymedicine.medical_treatmentPopulationPhysiologySettore MED/10 - Malattie Dell'Apparato RespiratorioModels BiologicalInsulin resistanceSleep Apnea SyndromesDiabetes mellitusInternal medicineGlucose IntoleranceMedicineAnimalsHumansContinuous positive airway pressureObesityeducationSleep restrictionAgedInflammationeducation.field_of_studybusiness.industryIntermittent hypoxiaMiddle Agedmedicine.diseaseObesityrespiratory tract diseasesEndocrinologyDiabetes insulin resistance intermittent hypoxia obesity sleep sleep apnoeaAdipose TissueFemaleMetabolic syndromeInsulin ResistancebusinessSleepThe European respiratory journal
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