2019
Obesity-associated, but not obesity-independent, tumors respond to insulin by increasing mitochondrial glucose oxidation
Rabin-Court A, Rodrigues MR, Zhang XM, Perry RJ. Obesity-associated, but not obesity-independent, tumors respond to insulin by increasing mitochondrial glucose oxidation. PLOS ONE 2019, 14: e0218126. PMID: 31188872, PMCID: PMC6561592, DOI: 10.1371/journal.pone.0218126.Peer-Reviewed Original ResearchMeSH KeywordsAlanineBreast NeoplasmsCell Line, TumorCitrate (si)-SynthaseColonic NeoplasmsFemaleGene Expression RegulationGlucoseGlutamic AcidHumansInsulinIsotope LabelingKetone OxidoreductasesLymphoma, B-CellMaleMelanomaMitochondriaObesityOrgan SpecificityOxidation-ReductionPhosphorylationProstatic NeoplasmsReceptor, InsulinSignal TransductionSkin NeoplasmsSmall Cell Lung CarcinomaConceptsCell divisionTumor cell linesCell linesMitochondrial glucose oxidationTumor typesObesity-driven insulin resistanceSubstrate preferenceMolecular mechanismsDose-dependent increaseGlucose oxidationPhysiologic insulinPyruvate dehydrogenase fluxWorse prognosisInsulin resistanceStable isotope methodObesityOxidative responsePhysiologic concentrationsSynthase fluxInsulinMetabolic signaturesTumor cellsTumorsDivisionLines
2018
Leptin Mediates a Glucose-Fatty Acid Cycle to Maintain Glucose Homeostasis in Starvation
Perry RJ, Wang Y, Cline GW, Rabin-Court A, Song JD, Dufour S, Zhang XM, Petersen KF, Shulman GI. Leptin Mediates a Glucose-Fatty Acid Cycle to Maintain Glucose Homeostasis in Starvation. Cell 2018, 172: 234-248.e17. PMID: 29307489, PMCID: PMC5766366, DOI: 10.1016/j.cell.2017.12.001.Peer-Reviewed Original Research