Search results for "glucose"

showing 10 items of 1206 documents

Modulating Oxidant Levels to Promote Healthy Aging

2020

Significance: Free radicals although originally thought of as damaging molecules, inevitable side effects of the utilization of oxygen by cells, are now considered as signals that by modifying, among others, the thiol-disulfide balance regulate many cell processes from metabolism to cell cycle. Recent Advances: This review discusses the importance of the modulation of the oxidant levels through physiological strategies such as physical exercise or genetic manipulations such as the overexpression of antioxidant enzymes, in the promotion of healthy aging. Critical Issues: We have divided the review into five different sections. In the first two sections of the article "Oxidants are signals" a…

0301 basic medicineAgingAntioxidantPhysiologymedia_common.quotation_subjectmedicine.medical_treatment[SDV]Life Sciences [q-bio]Clinical BiochemistryPhysical exerciseMitochondrionBiologyBiochemistryGene Expression Regulation EnzymologicHealthy Aging03 medical and health sciencesmedicineAnimalsHumansskeletal muscleMuscle SkeletalMolecular BiologyGeneral Environmental Sciencemedia_commonchemistry.chemical_classificationReactive oxygen species030102 biochemistry & molecular biologyexerciseHormesisLongevitySkeletal muscleCell BiologyOxidantshealth spanCell biologymitochondriaOxidative Stress030104 developmental biologymedicine.anatomical_structurechemistryMitochondrial biogenesisglucose-6-phosphate dehydrogenaseGeneral Earth and Planetary SciencesReactive Oxygen SpeciesOxidation-Reduction
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Overexpression of glucose 6 phosphate dehydrogenase preserves mouse pancreatic beta cells function until late in life.

2021

NAD(P)H donates electrons for reductive biosynthesis and antioxidant defense across all forms of life. Glucose-6- phosphate dehydrogenase (G6PD) is a critical enzyme to provide NADPH. G6PD deficiency is present in more than 400 million people worldwide. This enzymopathy provides protection against malaria but sensitizes cells to oxidative stressors. Oxidative stress has been involved in the pathogenesis of the diabetic complications and several studies have provided evidences of a link between G6PD deficiency and type 2 diabetes (T2D). We hypothesized that a moderate overexpression of G6PD (G6PD-Tg) could protect β-cells from age-associated oxidative stress thus reducing the risk of develop…

0301 basic medicineAgingmedicine.medical_specialtyOxidative phosphorylationType 2 diabetesGlucosephosphate Dehydrogenasemedicine.disease_causeBiochemistry03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicinehemic and lymphatic diseasesPhysiology (medical)Internal medicineDiabetes mellitusInsulin-Secreting Cellsparasitic diseasesNADPHmedicineGlucose-6-phosphate dehydrogenaseAnimalsPancreatic isletsDiabetesWild typenutritional and metabolic diseasesmedicine.diseaseOxidative Stress030104 developmental biologyEndocrinologymedicine.anatomical_structureGlucosephosphate Dehydrogenase DeficiencychemistryDiabetes Mellitus Type 2Oxidative stressPancreas030217 neurology & neurosurgeryOxidative stressFree radical biologymedicine
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Increased Body Weight and Fat Mass After Subchronic GIP Receptor Antagonist, but Not GLP-2 Receptor Antagonist, Administration in Rats

2019

Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-2 (GLP-2) are hormones secreted from the enteroendocrine cells after a meal. They exert their actions through activation of G protein-coupled receptors (R), the GIPR and GLP-2R, respectively. Both have been reported to influence metabolism. The purpose of the study was to investigate the role of the hormones in the regulation of lipid and bone homeostasis by subchronic treatment with novel GIPR and GLP-2R antagonists. Rats were injected once daily with vehicle, GIPR, or GLP-2R antagonists for 3 weeks. Body weight, food intake, body composition, plasma lipoprotein lipase (LPL), adipokines, triglycerides and the mark…

0301 basic medicineAgonistmedicine.medical_specialtyendocrine systemmedicine.drug_classEndocrinology Diabetes and MetabolismAdipokine030209 endocrinology & metabolismSettore BIO/09 - Fisiologialcsh:Diseases of the endocrine glands. Clinical endocrinologyBone resorption03 medical and health sciencesEndocrinology0302 clinical medicineInternal medicinemedicineglucagon-like peptide-2 (GLP-2)ReceptorOriginal Researchlcsh:RC648-665ChemistryLeptindigestive oral and skin physiologyAntagonistGIP receptorGIP receptor antagonistReceptor antagonistlipid homeostasis030104 developmental biologyEndocrinologyglucose-dependent insulinotropic polypeptide (GIP)hormones hormone substitutes and hormone antagonistsHormoneFrontiers in Endocrinology
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Direct Sensing of Nutrients via a LAT1-like Transporter in Drosophila Insulin-Producing Cells

2016

Summary Dietary leucine has been suspected to play an important role in insulin release, a hormone that controls satiety and metabolism. The mechanism by which insulin-producing cells (IPCs) sense leucine and regulate insulin secretion is still poorly understood. In Drosophila, insulin-like peptides (DILP2 and DILP5) are produced by brain IPCs and are released in the hemolymph after leucine ingestion. Using Ca2+-imaging and ex vivo cultured larval brains, we demonstrate that IPCs can directly sense extracellular leucine levels via minidiscs (MND), a leucine transporter. MND knockdown in IPCs abolished leucine-dependent changes, including loss of DILP2 and DILP5 in IPC bodies, consistent wit…

0301 basic medicineAmino Acid Transport Systemsheavy-chainmedicine.medical_treatmentInsulinsamino acid transporter0302 clinical medicinegenetics [Drosophila Proteins]cytology [Drosophila melanogaster]Glutamate DehydrogenaseHemolymphInsulin-Secreting Cellsmetabolism [Drosophila melanogaster]HemolymphDrosophila;Drosophila insulin-like peptides;amino acid transporter;food;glutamate dehydrogenase;glycemia;growth;insulin-producing cells;minidiscs;starvationDrosophila ProteinsProtein Isoformsmetabolism [Calcium]genetics [Insulins]genetics [Amino Acid Transport Systems]lcsh:QH301-705.5minidiscsGene knockdowncytology [Larva]pancreatic beta-cellglutamate dehydrogenaseBrainmetabolism [Hemolymph]secretionDrosophila melanogasterBiochemistryLarvaAlimentation et NutritionDrosophilaLeucineSignal Transductionglucose-transportgenetics [Glutamate Dehydrogenase]genetics [Protein Isoforms]growthamino-acidsmetabolism [Drosophila Proteins][SDV.BC]Life Sciences [q-bio]/Cellular BiologyNutrient sensingmetabolism [Larva]Biologyinsulin-producing cellsArticleGeneral Biochemistry Genetics and Molecular Biologymetabolism [Amino Acid Transport Systems]metabolism [Insulins]03 medical and health sciencesLeucineparasitic diseasesmedicineFood and NutritionAnimalsddc:610cytology [Insulin-Secreting Cells]cardiovascular diseasesAmino acid transporterMnd protein Drosophilaadministration & dosage [Leucine]metabolism [Protein Isoforms]Ilp5 protein Drosophilacytology [Brain]foodGlutamate dehydrogenaseInsulinNeurosciencesstarvationGlucose transportermetabolism [Insulin-Secreting Cells]glutamate-dehydrogenasel-leucineglycemia030104 developmental biologyGene Expression Regulationlcsh:Biology (General)metabolism [Brain]metabolism [Glutamate Dehydrogenase]Neurons and Cognitionmetabolism [Leucine]CalciumDrosophila insulin-like peptidesmetabolismfat-cells030217 neurology & neurosurgeryCell Reports
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In vitro effects of vitamins C and E, n-3 and n-6 PUFA and n-9 MUFA on placental cell function and redox status in type 1 diabetic pregnant women.

2016

IF 2.972; International audience; The aim of this investigation was to determine the in vitro effects of vitamin C and E, n-3 and n-6 PUFA and n-9 MUFA on placental cell proliferation and function in type 1 diabetes. Placenta tissues were collected from 30 control healthy and 30 type 1 diabetic women at delivery. Placental cells were isolated and were cultured in RPMI medium supplemented with vitamin C (50 μM), vitamin E (50 μM), n-3 PUFA (100 μM), n-6 PUFA (100 μM) or n-9 MUFA (100 μM). Cell proliferation, cell glucose uptake and intracellular oxidative status were investigated. Our results showed that basal placental cell proliferation, glucose uptake, malondialdehyde (MDA) and carbonyl p…

0301 basic medicineAntioxidantGlucose uptakemedicine.medical_treatmentPlacentaProliferationPregnancy in DiabeticsAscorbic Acidmedicine.disease_causeAntioxidantsFatty Acids Monounsaturatedchemistry.chemical_compound0302 clinical medicinePregnancyMalondialdehydeVitamin EVitamin C[ SDV.MHEP.GEO ] Life Sciences [q-bio]/Human health and pathology/Gynecology and obstetrics030219 obstetrics & reproductive medicineTrophoblastObstetrics and Gynecologyfood and beveragesCatalasemedicine.anatomical_structureType 1 diabetes[ SDV.BDLR ] Life Sciences [q-bio]/Reproductive BiologyHypertensionFemalelipids (amino acids peptides and proteins)Oxidant/antioxidant statusOxidation-ReductionIntracellularPolyunsaturated fatty-acidsVitaminAdultRiskmedicine.medical_specialtyPlacental cellsBiology03 medical and health sciencesYoung AdultInternal medicinePlacentaFatty Acids Omega-6Fatty Acids Omega-3medicineHumans[ SDV.BDD ] Life Sciences [q-bio]/Development BiologyCell ProliferationVitamin CSuperoxide DismutaseVitamin EMellitusPreeclampsiaDiet030104 developmental biologyEndocrinologyDiabetes Mellitus Type 1MetabolismReproductive MedicinechemistryOxidative stressOxidative stressPUFADevelopmental Biology
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Safe neoadjuvant trastuzumab-based treatment in HER2 + inflammatory early breast cancer in a glucose 6-phosphate dehydrogenase-deficient postmenopaus…

2019

Introduction Glucose 6-phosphate dehydrogenase (G6PD) is a basic antioxidant pathway for erythrocytes, being its deficiency the most common gene mutation worldwide. As breast cancer is one of the most frequent tumors, many of these patients may present with G6PD deficiency prior treatment without notice. Case report We present the case of a woman deficient for G6PD with the diagnosis of Stage IIIB (cT4d cN1 cM0) HER2-enriched early breast cancer. Management and outcome The patient underwent neoadjuvance with trastuzumab and anthracycline-free chemotherapy, based on docetaxel (75 mg/m2, 120 mg) and carboplatin (AUC 5, 560 mg). She did not present hemolytic crisis and no blood transfusions we…

0301 basic medicineAntioxidantReceptor ErbB-2medicine.medical_treatmentCommon geneBreast NeoplasmsDehydrogenasemedicine.disease_cause03 medical and health scienceschemistry.chemical_compoundAntineoplastic Agents Immunological0302 clinical medicineBreast cancerTrastuzumabmedicineHumansGlucose-6-phosphate dehydrogenasePharmacology (medical)skin and connective tissue diseasesAgedEarly breast cancerMutationbusiness.industryTrastuzumabmedicine.diseaseNeoadjuvant TherapyPostmenopauseGlucosephosphate Dehydrogenase DeficiencyTreatment Outcome030104 developmental biologyOncologychemistry030220 oncology & carcinogenesisCancer researchFemalebusinessmedicine.drugJournal of Oncology Pharmacy Practice
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Cardiolipin synthesis in brown and beige fat mitochondria is essential for systemic energy homeostasis

2018

Summary Activation of energy expenditure in thermogenic fat is a promising strategy to improve metabolic health, yet the dynamic processes that evoke this response are poorly understood. Here we show that synthesis of the mitochondrial phospholipid cardiolipin is indispensable for stimulating and sustaining thermogenic fat function. Cardiolipin biosynthesis is robustly induced in brown and beige adipose upon cold exposure. Mimicking this response through overexpression of cardiolipin synthase (Crls1) enhances energy consumption in mouse and human adipocytes. Crls1 deficiency in thermogenic adipocytes diminishes inducible mitochondrial uncoupling and elicits a nuclear transcriptional respons…

0301 basic medicineBiologiaBioenergeticsChop-10 ; Crls1 ; Beige Adipose ; Brown Adipose ; Cardiolipin ; Insulin Resistance ; Lipid Metabolism ; Mitochondria ; Phospholipids ; ThermogenesisPhysiologyGlucose uptakeAdipose tissueTransferases (Other Substituted Phosphate Groups)MitochondrionEnergy homeostasischemistry.chemical_compoundMice0302 clinical medicineAdipose Tissue Browninsulin resistancelipid metabolismCardiolipinAdipocytesCells CulturedThermogenesisthermogenesisCell biologyMitochondriamitochondriaCHOP-10lipids (amino acids peptides and proteins)BioquímicaCardiolipinsbeige adiposeArticle03 medical and health sciencesInsulin resistanceCRLS1medicineAnimalsHumansMolecular Biologyphospholipidsbrown adiposeMembrane ProteinsCell BiologyAdipose Tissue Beigemedicine.diseaseMice Inbred C57BL030104 developmental biologychemistrycardiolipinEnergy MetabolismThermogenesis030217 neurology & neurosurgery
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Mast cells contribute to autoimmune diabetes by releasing interleukin-6 and failing to acquire a tolerogenic IL-10+ phenotype

2017

Mast cells (MCs) are innate immune cells that exert positive and negative immune modulatory functions capable to enhance or limit the intensity and/or duration of adaptive immune responses. Although MCs are crucial to regulate T cell immunity, their action in the pathogenesis of autoimmune diseases is still debated. Here we demonstrate that MCs play a crucial role in T1D pathogenesis so that their selective depletion in conditional MC knockout NOD mice protects them from the disease. MCs of diabetic NOD mice are overly inflammatory and secrete large amounts of IL-6 that favors differentiation of IL-17-secreting T cells at the site of autoimmunity. Moreover, while MCs of control mice acquire…

0301 basic medicineBlood GlucoseAutoimmune diabeteAutoimmunityNodmedicine.disease_causeT-Lymphocytes RegulatoryAutoimmunityImmune toleranceSettore MED/13 - EndocrinologiaMiceAutoimmune diabetes0302 clinical medicineMice Inbred NODImmunology and AllergyNOD miceMice KnockoutInterleukin-17Forkhead Transcription FactorsFlow CytometryImmunohistochemistryhumanitiesInterleukin-10Interleukin 10Tumor necrosis factor alphaImmunologySettore MED/50 - Scienze Tecniche Mediche ApplicateMice TransgenicLaser Capture MicrodissectionReal-Time Polymerase Chain Reactionbehavioral disciplines and activities03 medical and health sciencesIslets of LangerhansImmune systemChymasesmedicineAnimalsInflammationInnate immune systembusiness.industryInterleukin-6Immune toleranceSettore MED/46 - Scienze Tecniche di Medicina di LaboratorioAutoimmune diabetes; Immune tolerance; Interleukin-10; Interleukin-6; Mast cells030104 developmental biologyDiabetes Mellitus Type 1ImmunologyMast cellsTh17 CellsMast cells; Autoimmune diabetes; Interleukin-6; Immune tolerance; Interleukin-10business030215 immunology
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Serum Amino Acid Profiles in Childhood Predict Triglyceride Level in Adulthood: A 7-Year Longitudinal Study in Girls.

2016

AbstractContext:Branched-chain and aromatic amino acids are associated with high risk of developing dyslipidemia and type II diabetes in adults.Objective:This study aimed to examine whether serum amino acid profiles associate with triglyceride concentrations during pubertal growth and predict hypertriglyceridemia in early adulthood.Design:This was a 7.5-year longitudinal study.Setting:The study was conducted at the Health Science Laboratory, University of Jyväskylä.Participants:A total of 396 nondiabetic Finnish girls aged 11.2 ± 0.8 years at the baseline participated in the study.Main Outcome Measures:Body composition was assessed by dual-energy x-ray absorptiometry; serum concentrations o…

0301 basic medicineBlood GlucoseLongitudinal studymedicine.medical_specialtyMagnetic Resonance SpectroscopyAdolescentEndocrinology Diabetes and Metabolismmedicine.medical_treatmentClinical BiochemistryContext (language use)030204 cardiovascular system & hematologyBiochemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineEndocrinologyAbsorptiometry PhotonInternal medicinemedicineHumansInsulinLongitudinal StudiesAmino AcidsChildTriglyceridesTriglyceridebusiness.industryInsulinBiochemistry (medical)Hypertriglyceridemiamedicine.disease030104 developmental biologyEndocrinologychemistryBody CompositionFemaleIsoleucineLeucinebusinessDyslipidemiaThe Journal of clinical endocrinology and metabolism
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New 1,4-Dihydropyridines Down-regulate Nitric Oxide in Animals with Streptozotocin-induced Diabetes Mellitus and Protect Deoxyribonucleic Acid agains…

2015

Diabetes mellitus (DM) and its complications cause numerous health and social problems throughout the world. Pathogenic actions of nitric oxide (NO) are responsible to a large extent for development of complications of DM. Search for compounds regulating NO production in patients with DM is thus important for the development of pharmacological drugs. Dihydropyridines (1,4-DHPs) are prospective compounds from this point of view. The goals of this study were to study the in vivo effects of new DHPs on NO and reactive nitrogen and oxygen species production in a streptozotocin (STZ)-induced model of DM in rats and to study their ability to protect DNA against nocive action of peroxynitrite. STZ…

0301 basic medicineBlood GlucoseMaleDihydropyridinesNitric Oxide Synthase Type IIIXanthine DehydrogenaseDown-RegulationNitric Oxide Synthase Type IIDHPS030204 cardiovascular system & hematologyPharmacologyToxicologyEndothelial NOSKidneyNitric OxideProtective AgentsNitric oxideDiabetes Mellitus Experimental03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePeroxynitrous AcidmedicineAnimalsRats WistarReactive nitrogen speciesPharmacologybiologyGeneral MedicineDNAStreptozotocinReactive Nitrogen SpeciesRatsNitric oxide synthasePeroxynitrous acid030104 developmental biologyBiochemistrychemistryLiverbiology.proteinReactive Oxygen SpeciesPeroxynitritemedicine.drugBasicclinical pharmacologytoxicology
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