2024
Deficits in brain glucose transport among younger adults with obesity
Gunawan F, Matson B, Coppoli A, Jiang L, Ding Y, Perry R, Sanchez‐Rangel E, DeAguiar R, Behar K, Rothman D, Mason G, Hwang J. Deficits in brain glucose transport among younger adults with obesity. Obesity 2024, 32: 1329-1338. PMID: 38764181, DOI: 10.1002/oby.24034.Peer-Reviewed Original ResearchBrain glucose transportLean participantsMarkers of insulin resistanceMagnetic resonance spectroscopy scansEffect of obesityAssociated with alterationsLong-term brain functionCerebral glucose metabolic rateGlucose transportGlucose metabolic rateCardiometabolic comorbiditiesBrain energy utilizationPeripheral markersHyperglycemic clampInsulin resistanceObesityBrain glucose uptakeHuman findingsEating behaviorsYounger ageYoung healthy participantsNeurocognitive functionGlucose transport capacityBrain functionNonesterified fatty acidsMetabolic underpinnings of cancer-related fatigue
Zhang X, Perry R. Metabolic underpinnings of cancer-related fatigue. AJP Endocrinology And Metabolism 2024, 326: e290-e307. PMID: 38294698, DOI: 10.1152/ajpendo.00378.2023.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsCancer-related fatigueMechanisms of cancer-related fatigueInsulin resistanceImpact of obesityCancer-induced painComplication of cancerTarget obesityInduce chronic inflammationObesityNarrative reviewObesity/insulin resistanceTumor growthChronic inflammationDetrimental complicationsCancer patientsMetabolic alterationsClinical researchNeuroendocrinological disturbancesMetabolic underpinningsAnalyzed recent studiesInsulinFatigueBehavioral disruptionPatientsPotential mechanisms
2023
The impact of variance in carnitine palmitoyltransferase-1 expression on breast cancer prognosis is stratified by clinical and anthropometric factors
Liu R, Ospanova S, Perry R. The impact of variance in carnitine palmitoyltransferase-1 expression on breast cancer prognosis is stratified by clinical and anthropometric factors. PLOS ONE 2023, 18: e0281252. PMID: 36735704, PMCID: PMC9897541, DOI: 10.1371/journal.pone.0281252.Peer-Reviewed Original ResearchConceptsBreast cancer prognosisBreast cancerFatty acid metabolismCancer prognosisCarnitine palmitoyltransferase 1 expressionHigh-risk breast cancerPre-menopausal patientsAcid metabolismPatient survival probabilityPositron emission tomography-computed tomography (PET-CT) imagesFatty acid oxidationMenopausal statusAnthropometric factorsPathogenic factorsCPT1A expressionRate-limiting enzymeObesityProtective relationshipCancerSurvival probabilityCancer Imaging ArchivePotential rolePatientsPrognosisAcid oxidation
2022
Insulin and cancer: a tangled web
Leitner BP, Siebel S, Akingbesote ND, Zhang X, Perry RJ. Insulin and cancer: a tangled web. Biochemical Journal 2022, 479: 583-607. PMID: 35244142, PMCID: PMC9022985, DOI: 10.1042/bcj20210134.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus Statements
2020
The Impact of Obesity on Tumor Glucose Uptake in Breast and Lung Cancer
Leitner BP, Perry RJ. The Impact of Obesity on Tumor Glucose Uptake in Breast and Lung Cancer. JNCI Cancer Spectrum 2020, 4: pkaa007. PMID: 32368718, PMCID: PMC7190208, DOI: 10.1093/jncics/pkaa007.Peer-Reviewed Original ResearchBody mass indexTumor glucose uptakeLung cancerGlucose uptakeGlucose metabolismNon-small cell lung cancerHigher body mass indexObesity-cancer linkImpact of obesityCell lung cancerSquamous cell carcinomaSoft tissue sarcomasAltered glucose metabolismPoor clinical prognosisTumor glucose metabolismMass indexPoor outcomeTissue sarcomasCell carcinomaTomography/Clinical prognosisBreast cancerProtective effectObesityCancer
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
Uncoupling Hepatic Oxidative Phosphorylation Reduces Tumor Growth in Two Murine Models of Colon Cancer
Wang Y, Nasiri AR, Damsky WE, Perry CJ, Zhang XM, Rabin-Court A, Pollak MN, Shulman GI, Perry RJ. Uncoupling Hepatic Oxidative Phosphorylation Reduces Tumor Growth in Two Murine Models of Colon Cancer. Cell Reports 2018, 24: 47-55. PMID: 29972790, PMCID: PMC6056247, DOI: 10.1016/j.celrep.2018.06.008.Peer-Reviewed Original ResearchConceptsControlled-release mitochondrial protonophoreTumor growthGlucose uptakeDiet-induced obesityMurine colon cancer modelColon cancer modelHepatic energy metabolismColon cancer pathogenesisHormonal milieuPlasma insulinFed miceInsulin infusionMurine modelColon cancerCancer modelCancer pathogenesisOxidative phosphorylationNeoplastic growthMitochondrial protonophoreHepatic oxidative phosphorylationObesityUnderlying mechanismEnergy metabolismCancerInsulin
2016
Acetate mediates a microbiome–brain–β-cell axis to promote metabolic syndrome
Perry RJ, Peng L, Barry NA, Cline GW, Zhang D, Cardone RL, Petersen KF, Kibbey RG, Goodman AL, Shulman GI. Acetate mediates a microbiome–brain–β-cell axis to promote metabolic syndrome. Nature 2016, 534: 213-217. PMID: 27279214, PMCID: PMC4922538, DOI: 10.1038/nature18309.Peer-Reviewed Original ResearchConceptsGut microbiotaMetabolic syndromeGlucose-stimulated insulin secretionAltered gut microbiotaParasympathetic nervous systemPossible therapeutic targetGhrelin secretionInsulin resistanceInsulin secretionParasympathetic activationTherapeutic targetNervous systemObesityMicrobiota interactionsSyndromeMicrobiotaSecretionActivationSequelaeHyperphagia