2020
Nesfatin-1 decreases the motivational and rewarding value of food
Dore R, Krotenko R, Reising JP, Murru L, Sundaram SM, Di Spiezio A, Müller-Fielitz H, Schwaninger M, Jöhren O, Mittag J, Passafaro M, Shanabrough M, Horvath TL, Schulz C, Lehnert H. Nesfatin-1 decreases the motivational and rewarding value of food. Neuropsychopharmacology 2020, 45: 1645-1655. PMID: 32353862, PMCID: PMC7419560, DOI: 10.1038/s41386-020-0682-3.Peer-Reviewed Original ResearchMeSH KeywordsCalcium-Binding ProteinsDNA-Binding ProteinsMotivationNerve Tissue ProteinsNucleobindinsRewardConceptsNUCB2/nesfatinNesfatin-1Nucleobindin-2Food intakeNesfatin-1 actionDopaminergic neuron activityFasting-induced increaseReward-related brain areasOutward potassium currentHedonic pathwaysHedonic feedingGABA neuronsLeptin resistanceBrain areasPotassium currentNeuron activityFood rewardEnergy intakeReward circuitryElectrophysiological recordingsNesfatinCentral administrationEnhanced sensitizationIntakeHomeostatic mechanisms
2018
Loss of Nucleobindin-2 Causes Insulin Resistance in Obesity without Impacting Satiety or Adiposity
Ravussin A, Youm YH, Sander J, Ryu S, Nguyen K, Varela L, Shulman GI, Sidorov S, Horvath TL, Schultze JL, Dixit VD. Loss of Nucleobindin-2 Causes Insulin Resistance in Obesity without Impacting Satiety or Adiposity. Cell Reports 2018, 24: 1085-1092.e6. PMID: 30067966, PMCID: PMC6223120, DOI: 10.1016/j.celrep.2018.06.112.Peer-Reviewed Original ResearchMeSH KeywordsAdiposityAnimalsDiet, High-FatEatingInsulin ResistanceMacrophagesMiceNF-kappa BNucleobindinsObesitySatiationConceptsHigh-fat dietInsulin resistanceFood intakeMetabolic inflammationNucleobindin-2M2-like macrophage polarizationHigh-fat diet feedingWeight lossAdipose tissue macrophagesObesity-associated diseasesNesfatin-1Insulin sensitivityDiet feedingMacrophage polarizationNUCB2 proteinMyeloid cellsTissue macrophagesGlobal deletionClassical M1NUCB2NFκB-dependent mannerWeight gainSatietyIntakeAdiposity
2009
Nesfatin-1-Regulated Oxytocinergic Signaling in the Paraventricular Nucleus Causes Anorexia through a Leptin-Independent Melanocortin Pathway
Maejima Y, Sedbazar U, Suyama S, Kohno D, Onaka T, Takano E, Yoshida N, Koike M, Uchiyama Y, Fujiwara K, Yashiro T, Horvath TL, Dietrich MO, Tanaka S, Dezaki K, Oh-I S, Hashimoto K, Shimizu H, Nakata M, Mori M, Yada T. Nesfatin-1-Regulated Oxytocinergic Signaling in the Paraventricular Nucleus Causes Anorexia through a Leptin-Independent Melanocortin Pathway. Cell Metabolism 2009, 10: 355-365. PMID: 19883614, DOI: 10.1016/j.cmet.2009.09.002.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnorexiaAutocrine CommunicationCalcium-Binding ProteinsDNA-Binding ProteinsLeptinMelanocortinsMiceNerve Tissue ProteinsNeuroendocrine CellsNucleobindinsOxytocinParacrine CommunicationParaventricular Hypothalamic NucleusPro-OpiomelanocortinRatsRats, ZuckerSignal TransductionSolitary NucleusConceptsNucleus tractus solitariusNesfatin-1Oxytocin releaseParacrine/autocrine actionsNesfatin-1 neuronsParaventricular nucleus functionPro-opiomelanocortin (POMC) neuronsZucker fatty ratsOxytocin receptor antagonistOxytocin terminalsPVN neuronsTractus solitariusReceptor antagonistCentral injectionParaventricular nucleusAutocrine actionMelanocortin pathwayNeuronal activityNeural pathwaysPVNAnorexiaNeuronsNucleus functionOxytocinImmunoelectron micrographs