2024
Skeletal muscle TET3 promotes insulin resistance through destabilisation of PGC-1α
Liu B, Xie D, Huang X, Jin S, Dai Y, Sun X, Li D, Bennett A, Diano S, Huang Y. Skeletal muscle TET3 promotes insulin resistance through destabilisation of PGC-1α. Diabetologia 2024, 67: 724-737. PMID: 38216792, PMCID: PMC10904493, DOI: 10.1007/s00125-023-06073-5.Peer-Reviewed Original ResearchConceptsTen-eleven translocationMuscle insulin sensitivityRNA-seqPGC-1aRegulation of muscle insulin sensitivityType 2 diabetesAnalysis of RNA-seqResponse to environmental cuesGenome-wide expression profilingWild-typeHFD-fedHFD-induced insulin resistanceHigh-fat diet (HFD)-inducedExpression levelsMaintenance of glucoseSkeletal muscle insulin sensitivityAccession numbersSkeletal muscleEnhanced glucose toleranceFamily dioxygenasesMitochondrial respirationSkeletal muscle of humansEnvironmental cuesMitochondrial functionBiological processes
2023
Microglia in Central Control of Metabolism
Kim J, Copperi F, Diano S. Microglia in Central Control of Metabolism. Physiology 2023, 39: 5-17. PMID: 37962895, PMCID: PMC11283896, DOI: 10.1152/physiol.00021.2023.Peer-Reviewed Original Research146-OR: Causative Role of Hypothalamic Ventromedial Glucose-Inhibited Neurons in Impaired Counterregulatory Responses to Hypoglycemia
COPPERI F, SHEN X, DIANO S. 146-OR: Causative Role of Hypothalamic Ventromedial Glucose-Inhibited Neurons in Impaired Counterregulatory Responses to Hypoglycemia. Diabetes 2023, 72 DOI: 10.2337/db23-146-or.Peer-Reviewed Original ResearchImpaired counterregulatory responseCounterregulatory responsesGI neuronsRecurrent hypoglycemiaCausative roleGlucose-inhibited neuronsType 1 diabetesBlood glucose levelsScientific evidence pointsDiabetes CenterChemogenetic activationKidney diseaseVentromedial nucleusNeuronal activationGlucose levelsMouse modelCurrent evidenceConsecutive daysMiceNeuronsAdministrationSignificant decreaseCausal involvementNational InstituteHypoglycemia
2017
POMC Neurons: From Birth to Death
Toda C, Santoro A, Kim JD, Diano S. POMC Neurons: From Birth to Death. Annual Review Of Physiology 2017, 79: 209-236. PMID: 28192062, PMCID: PMC5669621, DOI: 10.1146/annurev-physiol-022516-034110.Peer-Reviewed Original ResearchConceptsPro-opiomelanocortin (POMC) neuronsHypothalamic neuronal populationsPOMC neuronsBrain stemHypothalamic nucleiSpinal cordAutonomic regionsMelanocortin systemBrain areasNeuronal populationsNeuronal circuitsHomeostatic functionsBrain structuresPathological dysregulationHypothalamusCritical regulatorNeuronsPhysiological functionsCurrent understandingMajor roleCordDRP1 Suppresses Leptin and Glucose Sensing of POMC Neurons
Santoro A, Campolo M, Liu C, Sesaki H, Meli R, Liu ZW, Kim JD, Diano S. DRP1 Suppresses Leptin and Glucose Sensing of POMC Neurons. Cell Metabolism 2017, 25: 647-660. PMID: 28190775, PMCID: PMC5366041, DOI: 10.1016/j.cmet.2017.01.003.Peer-Reviewed Original ResearchConceptsPeroxisome proliferator-activated receptorPOMC neuronsLeptin sensitivityHypothalamic pro-opiomelanocortin (POMC) neuronsPro-opiomelanocortin (POMC) neuronsCounter-regulatory responseProliferator-activated receptorMitochondrial sizeFed miceGlucoprivic stimuliNeuronal activationFl/Glucose metabolismMetabolic environmentNeuronsFasted animalsIntracellular mechanismsReduced expressionGlucose responsivenessGreater activationInducible deletionROS productionMiceStrong inhibitionMitochondrial fission regulator
2016
UCP2 Regulates Mitochondrial Fission and Ventromedial Nucleus Control of Glucose Responsiveness
Toda C, Kim JD, Impellizzeri D, Cuzzocrea S, Liu ZW, Diano S. UCP2 Regulates Mitochondrial Fission and Ventromedial Nucleus Control of Glucose Responsiveness. Cell 2016, 164: 872-883. PMID: 26919426, PMCID: PMC4770556, DOI: 10.1016/j.cell.2016.02.010.Peer-Reviewed Original ResearchConceptsSystemic glucose homeostasisMitochondrial fissionCellular biological processesMitochondrial dynamicsGenetic manipulationGlucose homeostasisReactive oxygen speciesBiological processesMitochondrial adaptationsProtein 2Reduced reactive oxygen speciesOxygen speciesHomeostasisCritical roleMetabolic environmentGlucose-excited neuronsGlucose responsivenessFissionNeuronal circuitrySpeciesNeuronsRegulationVMH neuronsGlucose loadPool
2015
Hypothalamic POMC neurons promote cannabinoid-induced feeding
Koch M, Varela L, Kim JG, Kim JD, Hernández-Nuño F, Simonds SE, Castorena CM, Vianna CR, Elmquist JK, Morozov YM, Rakic P, Bechmann I, Cowley MA, Szigeti-Buck K, Dietrich MO, Gao XB, Diano S, Horvath TL. Hypothalamic POMC neurons promote cannabinoid-induced feeding. Nature 2015, 519: 45-50. PMID: 25707796, PMCID: PMC4496586, DOI: 10.1038/nature14260.Peer-Reviewed Original ResearchConceptsPOMC neuronsΒ-endorphinHypothalamic pro-opiomelanocortin (POMC) neuronsOpioid peptide β-endorphinHypothalamic POMC neuronsPromotion of feedingPro-opiomelanocortin (POMC) neuronsCannabinoid receptor 1CB1R activityPOMC activitySated miceHormone releaseHypothalamic administrationFood intakeCentral regulationNeuronal activityParadoxical increaseCB1RReceptor 1POMC cellsNeuronsMitochondrial adaptationsDecreased activityPOMC geneUnsuspected role
2010
Hypothalamic prolylcarboxypeptidase (PRCP) in the regulation of melanocortin system
Diano S. Hypothalamic prolylcarboxypeptidase (PRCP) in the regulation of melanocortin system. The Biomedical & Life Sciences Collection 2010, 2010: e1002473. DOI: 10.69645/zqwp1030.Peer-Reviewed Original Research
2001
Minireview: Ghrelin and the Regulation of Energy Balance—A Hypothalamic Perspective
Horvath T, Diano S, Sotonyi P, Heiman M, Tschöp M. Minireview: Ghrelin and the Regulation of Energy Balance—A Hypothalamic Perspective. Endocrinology 2001, 142: 4163-4169. DOI: 10.1210/en.142.10.4163.Peer-Reviewed Original ResearchGH secretionSynthetic ghrelin receptor agonistRegulation of GH secretionGhrelin receptor agonistEtiology of obesityEnergy homeostasisRegulate energy homeostasisGH secretagoguesReceptor agonistsLeptin actionClinical trialsGhrelinChronic changesNeuroendocrine networkPrevent energy deficitRegulation of metabolismNutritional stateCentral regulatorCentral regulator of metabolismSubject of ongoing discussionsRegulation of growth processesEnergy deficitSecretionHomeostasisStomach
2000
Mitochondrial Uncoupling Protein 2 (UCP2) in the Nonhuman Primate Brain and Pituitary**This work was supported by NSF Grant IBN-9728581, NIH Grants NS-36111, MH-59847, RR-00163, HD-29186, and HD-37186.
Diano S, Urbanski H, Horvath B, Bechmann I, Kagiya A, Nemeth G, Naftolin F, Warden C, Horvath T. Mitochondrial Uncoupling Protein 2 (UCP2) in the Nonhuman Primate Brain and Pituitary**This work was supported by NSF Grant IBN-9728581, NIH Grants NS-36111, MH-59847, RR-00163, HD-29186, and HD-37186. Endocrinology 2000, 141: 4226-4238. DOI: 10.1210/en.141.11.4226.Peer-Reviewed Original ResearchUncoupling protein 2Pituitary glandPrimate brainIn situ hybridization histochemistryMitochondrial uncoupling protein 2Mitochondrial uncoupling proteinMessenger RNAGH-producing cellsNonhuman primate brainTreatment of metabolic disordersBrain stem regionsUncoupling protein 2 expressionAxonal processesRegulatory componentsUncoupling proteinPrimate hypothalamusPOMC cellsMetabolic regulationArcuate nucleusHybridization histochemistryAnterior pituitaryMitochondrial oxidationStem regionNeuropeptide YPeptide expression3,5-Diiodo-l-Thyronine Regulates Glucose-6-Phosphate Dehydrogenase Activity in the Rat*
Lombardi A, Beneduce L, Moreno M, Diano S, Colantuoni V, Ursini M, Lanni A, Goglia F. 3,5-Diiodo-l-Thyronine Regulates Glucose-6-Phosphate Dehydrogenase Activity in the Rat*. Endocrinology 2000, 141: 1729-1734. DOI: 10.1210/en.141.5.1729.Peer-Reviewed Original ResearchMalic enzymeG6PD mRNA expressionInjection of T2Enzyme activityMessenger RNAG6PD messenger RNAG6PD activityGlucose-6-phosphate dehydrogenaseComplementary DNA probeGlucose-6-phosphateEffect of T3Enzyme regulationDNA probesActivities of lipogenic enzymesProtein synthesis inhibitorTranscript levelsLipogenic enzymesNorthern blottingGlucose-6-phosphate dehydrogenase activityMRNA expressionEnzymeEffects of T2G6PDDehydrogenase activityIopanoic acid treatment
1999
Interactions between Neuropeptide Y and γ -Aminobutyric Acid in Stimulation of Feeding: A Morphological and Pharmacological Analysis*
Pu S, Jain M, Horvath T, Diano S, Kalra P, Kalra S. Interactions between Neuropeptide Y and γ -Aminobutyric Acid in Stimulation of Feeding: A Morphological and Pharmacological Analysis*. Endocrinology 1999, 140: 933-940. DOI: 10.1210/en.140.2.933.Peer-Reviewed Original ResearchParaventricular nucleusStimulation of feedingNeuropeptide YG-aminobutyric acidFood intakeArcuate nucleusCoadministration of neuropeptide YNPY-induced food intakeSite of NPY actionEffects of muscimolGABAA receptor agonistDose-related fashionSubpopulations of NPY neuronsElectron microscopic double stainingRat brain sectionsFeeding responseSated ratsNPY neuronsReceptor agonistsNPY actionMessenger systemsMuscimolHypothalamic controlBrain stemGABA
1998
Fasting-Induced Increase in Type II Iodothyronine Deiodinase Activity and Messenger Ribonucleic Acid Levels Is Not Reversed by Thyroxine in the Rat Hypothalamus*
Diano S, Naftolin F, Goglia F, Horvath T. Fasting-Induced Increase in Type II Iodothyronine Deiodinase Activity and Messenger Ribonucleic Acid Levels Is Not Reversed by Thyroxine in the Rat Hypothalamus*. Endocrinology 1998, 139: 2879-2884. DOI: 10.1210/en.139.6.2879.Peer-Reviewed Original ResearchPTU-treated ratsThyroid glandShort-term fastingPropylthiouracil treatmentEuthyroid controlsThyroid hormonesEuthyroid animalsDeiodinase activityMessenger RNAFasted ratsAdjacent periventricular regionsMessenger ribonucleic acid levelsQuantitative in situ hybridization analysisHypothalamic paraventricular nucleusRelease of TRHGroups of fasted ratsT4-treated ratsLevels of thyroid hormonesHypothalamus of ratsDeclining plasma levelsRibonucleic acid levelsThyroid hormone levelsSerum thyroid hormonesFasting-induced increaseWeeks of PTU administration
1997
Evidence Showing That β-Endorphin Regulates Cyclic Guanosine 3′,5′-Monophosphate (cGMP) Efflux: Anatomical and Functional Support for an Interaction between Opiates and Nitric Oxide*
Pu S, Horvath T, Diano S, Naftolin F, Kalra P, Kalra S. Evidence Showing That β-Endorphin Regulates Cyclic Guanosine 3′,5′-Monophosphate (cGMP) Efflux: Anatomical and Functional Support for an Interaction between Opiates and Nitric Oxide*. Endocrinology 1997, 138: 1537-1543. DOI: 10.1210/en.138.4.1537.Peer-Reviewed Original ResearchN-methyl-D-aspartateExcitatory amino acidsCyclic guanosine 3',5'-monophosphateMedial preoptic areaOpioid influenceGnRH secretionNitric oxideExcitatory N-methyl-D-aspartateN-methyl-D-aspartate receptorsPreoptic areaInhibitory opioid influenceB-endorphinOpiate receptor antagonistNOS-immunoreactive neuronsPituitary LH secretionNO releaseStimulation of NO releaseRelease of GnRHSubpopulations of neuronsGuanosine 3',5'-monophosphateCentral nervous systemReceptor agonistsReceptor antagonistEndogenous opioidsHypothalamic sectionsGonadal Steroids Target AMPA Glutamate Receptor-Containing Neurons in the Rat Hypothalamus, Septum and Amygdala: A Morphological and Biochemical Study*
Diano S, Naftolin F, Horvath T. Gonadal Steroids Target AMPA Glutamate Receptor-Containing Neurons in the Rat Hypothalamus, Septum and Amygdala: A Morphological and Biochemical Study*. Endocrinology 1997, 138: 778-789. DOI: 10.1210/en.138.2.778.Peer-Reviewed Original ResearchIncreased levels of GluR1AMPA receptorsExcitatory neurotransmissionRegulatory effect of estradiolGonadal steroidsHypothalamic regionsExpression of AMPA receptorsExpression of glutamate receptorsLevels of GluR1Receptor-containing neuronsAMPA receptor expressionEffects of estradiolBed nucleusGluR2/3 expressionIncidence of colocalizationReceptor expressionFemale ratsEstradiol treatmentAndrogen receptorGlutamate receptorsRat hypothalamusEstrogen receptorHormonal milieuHypothalamic functionHypothalamic area