2018
The 7q11.23 Protein DNAJC30 Interacts with ATP Synthase and Links Mitochondria to Brain Development
Tebbenkamp ATN, Varela L, Choi J, Paredes MI, Giani AM, Song JE, Sestan-Pesa M, Franjic D, Sousa AMM, Liu ZW, Li M, Bichsel C, Koch M, Szigeti-Buck K, Liu F, Li Z, Kawasawa YI, Paspalas CD, Mineur YS, Prontera P, Merla G, Picciotto MR, Arnsten AFT, Horvath TL, Sestan N. The 7q11.23 Protein DNAJC30 Interacts with ATP Synthase and Links Mitochondria to Brain Development. Cell 2018, 175: 1088-1104.e23. PMID: 30318146, PMCID: PMC6459420, DOI: 10.1016/j.cell.2018.09.014.Peer-Reviewed Original ResearchConceptsCopy number variationsATP synthase dimersOxidative phosphorylation supercomplexesHuman neurodevelopmental disordersATP synthaseWS pathogenesisGene contributionMitochondrial featuresBrain developmentWilliams syndromeMitochondrial dysfunctionNeocortical pyramidal neuronsNeural phenotypesMitochondriaPyramidal neuronsMachineryMorphological featuresNeurodevelopmental disordersDysfunctionSupercomplexesPhenotypeMild Impairment of Mitochondrial OXPHOS Promotes Fatty Acid Utilization in POMC Neurons and Improves Glucose Homeostasis in Obesity
Timper K, Paeger L, Sánchez-Lasheras C, Varela L, Jais A, Nolte H, Vogt MC, Hausen AC, Heilinger C, Evers N, Pospisilik JA, Penninger JM, Taylor EB, Horvath TL, Kloppenburg P, Brüning JC. Mild Impairment of Mitochondrial OXPHOS Promotes Fatty Acid Utilization in POMC Neurons and Improves Glucose Homeostasis in Obesity. Cell Reports 2018, 25: 383-397.e10. PMID: 30304679, PMCID: PMC6349418, DOI: 10.1016/j.celrep.2018.09.034.Peer-Reviewed Original ResearchConceptsPOMC neuronsApoptosis-inducing factorImproved glucose metabolismFatty acid utilizationDecrease firingPomc-CreFatty acid metabolismHFD feedingReactive oxygen species formationSystemic glucoseHypothalamic proopiomelanocortinLean miceMitochondrial respirationObese miceObese conditionsInsulin sensitivityGlucose homeostasisGlucose metabolismMild impairmentOxygen species formationFiring propertiesNeuronsOxidative phosphorylationMicePartial impairment
2015
Estrogen- and Satiety State-Dependent Metabolic Lateralization in the Hypothalamus of Female Rats
Toth I, Kiss DS, Jocsak G, Somogyi V, Toronyi E, Bartha T, Frenyo LV, Horvath TL, Zsarnovszky A. Estrogen- and Satiety State-Dependent Metabolic Lateralization in the Hypothalamus of Female Rats. PLOS ONE 2015, 10: e0137462. PMID: 26339901, PMCID: PMC4560379, DOI: 10.1371/journal.pone.0137462.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsElectron TransportEstradiolFastingFemaleFunctional LateralityHypothalamusMitochondriaOvariectomyOxidative PhosphorylationRatsRats, WistarSatiationConceptsAd libitum fed animalsFemale ratsRight-sided dominanceSatiety stateFed animalsOvariectomized female ratsContribution of estrogenMetabolic differencesHours of fastingIntensity of cellsState 3 mitochondrial respirationHypothalamic functionMetabolic asymmetryTissue metabolismHypothalamusEstrogenProportion of animalsHypothalamic asymmetryRatsAd libitumLateralizationHigher centersMitochondrial respiration rateEnergy metabolism
2009
The role of mitochondrial uncoupling proteins in lifespan
Dietrich MO, Horvath TL. The role of mitochondrial uncoupling proteins in lifespan. Pflügers Archiv - European Journal Of Physiology 2009, 459: 269-275. PMID: 19760284, PMCID: PMC2809791, DOI: 10.1007/s00424-009-0729-0.Peer-Reviewed Original ResearchConceptsMitochondrial inner membraneCellular biochemical reactionsMitochondrial uncoupling proteinProduction of ATPCellular functionsInner membraneSpecialized proteinsBreakdown of lipidsMain organellesExcess of ROSPhysiological uncouplingOxidative phosphorylationUncoupling proteinAdenosine triphosphateOxygen reactive speciesROS productionProteinEnergetic substratesBiochemical reactionsCellular damageMitochondriaROSIntermediate substrateUCPShed light