2024
Heterogeneity of hepatocyte dynamics restores liver architecture after chemical, physical or viral damage
Ruz-Maldonado I, Gonzalez J, Zhang H, Sun J, Bort A, Kabir I, Kibbey R, Suárez Y, Greif D, Fernández-Hernando C. Heterogeneity of hepatocyte dynamics restores liver architecture after chemical, physical or viral damage. Nature Communications 2024, 15: 1247. PMID: 38341404, PMCID: PMC10858916, DOI: 10.1038/s41467-024-45439-0.Peer-Reviewed Original Research
2020
NLRX1 Deletion Increases Ischemia-Reperfusion Damage and Activates Glucose Metabolism in Mouse Heart
Zhang H, Xiao Y, Nederlof R, Bakker D, Zhang P, Girardin SE, Hollmann MW, Weber NC, Houten SM, van Weeghel M, Kibbey RG, Zuurbier CJ. NLRX1 Deletion Increases Ischemia-Reperfusion Damage and Activates Glucose Metabolism in Mouse Heart. Frontiers In Immunology 2020, 11: 591815. PMID: 33362773, PMCID: PMC7759503, DOI: 10.3389/fimmu.2020.591815.Peer-Reviewed Original ResearchConceptsIschemia-reperfusion injuryNOD-like receptorsMouse heartsKO heartsGlucose metabolismCardiac ischemia-reperfusion injuryIschemia-reperfusion damageMin of reperfusionCardiac IR injurySurvival pathwaysPro-inflammatory memberCardiac glucose metabolismInnate immune systemCardiac oxygen consumptionFatty acid oxidationInflammatory parametersPyruvate dehydrogenase fluxIR injuryEarly reperfusionInflammatory mediatorsMin reperfusionSevere ischemiaC-palmitateImmune systemReperfusionEndocrine-Exocrine Signaling Drives Obesity-Associated Pancreatic Ductal Adenocarcinoma
Chung KM, Singh J, Lawres L, Dorans KJ, Garcia C, Burkhardt DB, Robbins R, Bhutkar A, Cardone R, Zhao X, Babic A, Vayrynen SA, Dias Costa A, Nowak JA, Chang DT, Dunne RF, Hezel AF, Koong AC, Wilhelm JJ, Bellin MD, Nylander V, Gloyn AL, McCarthy MI, Kibbey RG, Krishnaswamy S, Wolpin BM, Jacks T, Fuchs CS, Muzumdar MD. Endocrine-Exocrine Signaling Drives Obesity-Associated Pancreatic Ductal Adenocarcinoma. Cell 2020, 181: 832-847.e18. PMID: 32304665, PMCID: PMC7266008, DOI: 10.1016/j.cell.2020.03.062.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCarcinogenesisCarcinoma, Pancreatic DuctalCell LineCell Line, TumorCell Transformation, NeoplasticDisease Models, AnimalDisease ProgressionEndocrine CellsExocrine GlandsFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, Inbred C57BLMutationObesityPancreatic NeoplasmsSignal TransductionTumor MicroenvironmentConceptsPancreatic ductal adenocarcinomaPDAC progressionDuctal adenocarcinomaMajor modifiable risk factorModifiable risk factorsBeta cell expressionObesity-associated changesAutochthonous mouse modelPancreatic ductal tumorigenesisDriver gene mutationsPeptide hormone cholecystokininRisk factorsPDAC developmentMouse modelObesityHormone cholecystokininOncogenic KrasCell expressionTumor microenvironmentDietary inductionCancer developmentGene mutationsReversible roleMurine samplesProgression
2019
N-acyl taurines are endogenous lipid messengers that improve glucose homeostasis
Grevengoed TJ, Trammell SAJ, McKinney MK, Petersen N, Cardone RL, Svenningsen JS, Ogasawara D, Nexøe-Larsen CC, Knop FK, Schwartz TW, Kibbey RG, Cravatt BF, Gillum MP. N-acyl taurines are endogenous lipid messengers that improve glucose homeostasis. Proceedings Of The National Academy Of Sciences Of The United States Of America 2019, 116: 24770-24778. PMID: 31740614, PMCID: PMC6900532, DOI: 10.1073/pnas.1916288116.Peer-Reviewed Original ResearchMeSH KeywordsAmidohydrolasesAmino Acid SubstitutionAnimalsBlood GlucoseDisease Models, AnimalEatingEthanolaminesFemaleGlucagonGlucagon-Like Peptide 1Glucose Tolerance TestHumansInjections, IntravenousInsulinIslets of LangerhansMaleMetabolic SyndromeMiceMice, TransgenicMiddle AgedOleic AcidsPostprandial PeriodReceptors, G-Protein-CoupledTaurineConceptsFatty acid amide hydrolaseGLP-1 secretionPostprandial glucose regulationN-acyl taurinesBioactive fatty acid amidesEndogenous lipid messengersGlucagon secretionGlucose toleranceInsulin sensitivityUnique metabolic profileFood intakeGLP-1Peripheral tissuesMouse modelGlucose homeostasisLipid messengersGlucose regulationMetabolic diseasesAmide hydrolaseFunctional polymorphismsConcurrent elevationSubstantial elevationMetabolic profileFatty acid amidesMice
2017
Pathogenesis of hypothyroidism-induced NAFLD is driven by intra- and extrahepatic mechanisms
Ferrandino G, Kaspari RR, Spadaro O, Reyna-Neyra A, Perry RJ, Cardone R, Kibbey RG, Shulman GI, Dixit VD, Carrasco N. Pathogenesis of hypothyroidism-induced NAFLD is driven by intra- and extrahepatic mechanisms. Proceedings Of The National Academy Of Sciences Of The United States Of America 2017, 114: e9172-e9180. PMID: 29073114, PMCID: PMC5664516, DOI: 10.1073/pnas.1707797114.Peer-Reviewed Original ResearchConceptsNonalcoholic fatty liver diseaseDe novo lipogenesisAdipose tissue lipolysisHepatic insulin resistanceThyroid hormonesHypothyroid miceImpaired suppressionInsulin resistanceTissue lipolysisInsulin secretionHigh thyroid-stimulating hormone levelsRegulation of THThyroid-stimulating hormone levelsLipid utilizationFatty liver diseaseSerum glucose levelsEndogenous glucose productionLow thyroid hormoneFatty acidsHepatic lipid utilizationLiver diseaseSevere hypothyroidismHormone levelsProfound suppressionGlucose levels