Adjunct Faculty
Adjunct faculty typically have an academic or research appointment at another institution and contribute or collaborate with one or more School of Medicine faculty members or programs.
Adjunct rank detailsIkki Sakuma
Assistant Professor AdjunctAbout
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Assistant Professor Adjunct
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Endocrinology
Assistant Professor AdjunctPrimary
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Research at a Glance
Yale Co-Authors
Frequent collaborators of Ikki Sakuma's published research.
Publications Timeline
A big-picture view of Ikki Sakuma's research output by year.
Gerald I Shulman, MD, PhD, MACP, MACE, FRCP
Kitt Petersen, MD
Mario Kahn
Rafael Calais Gaspar, PhD, MSc
Brandon T. Hubbard
Dongyan Zhang
14Publications
116Citations
Publications
2026
LSD1 inhibitor, TAS1440, disrupts INSM1-LSD1 complex activating tumor-suppressive pathways via transcriptional reprogramming in neuroendocrine SCLC
Machida T, Gong Y, Tsukioka S, Onodera A, Nakayama A, Hashimoto N, Fuchigami T, Nishimura M, Ogino T, Kurimoto R, Uematsu Y, Suzuki H, Yu H, Chen M, Yokoyama M, Sakuma I, Taki Y, Kono T, Miki T, Motohashi S, Kawashima Y, Ohara O, Yamashita S, Suzuki T, Hatanaka R, Kodama Y, Ohkubo S, Tanaka T. LSD1 inhibitor, TAS1440, disrupts INSM1-LSD1 complex activating tumor-suppressive pathways via transcriptional reprogramming in neuroendocrine SCLC. Nature Communications 2026 PMID: 41881985, DOI: 10.1038/s41467-026-70984-1.Peer-Reviewed Original ResearchAltmetricConceptsSmall cell lung cancerCell lung cancerLimited treatment optionsLSD1 inhibitorsTumor suppressive pathwaysTumor regressionTreatment optionsLung cancerNeuroendocrine stateEpigenetic therapyTherapy candidatesLSD1 inhibitionOff-target effectsStructure-based engineeringHistone marksTranscriptional reprogrammingLSD1 activityChemoresistanceTherapyDinucleotide sitesINSM1InhibitorsMode of actionEnzymatic activityIrreversible inhibitorAxis-Specific Peripartum Management for Radiation-Induced Panhypopituitarism with AVP-D: A Case Report
Kono T, Miyagawa H, Kawauchi Y, Taki Y, Sakuma I, Hashimoto N, Oki Y, Shimatsu A, Tanaka T. Axis-Specific Peripartum Management for Radiation-Induced Panhypopituitarism with AVP-D: A Case Report. AACE Clinical Case Reports 2026 DOI: 10.1016/j.aed.2026.01.006.Peer-Reviewed Original ResearchConceptsCranial irradiationLevothyroxine dose adjustmentsSubcutaneous growth hormoneSecondary adrenal insufficiencyArginine vasopressin deficiencyIn vitro fertilizationICE chemotherapyOral desmopressinPeripartum courseCentral hypothyroidismAdrenal insufficiencyOral hydrocortisoneVasopressin deficiencyPeripartum managementThyroid replacementDose adjustmentPerinatal courseCase reportFree thyroxineGrowth hormoneReproductive medicineEndocrine profilePregnancy confirmationChemotherapyEndocrine axis
2025
Cideb knockdown in mice increases mitochondrial fat oxidation and reverses hepatic steatosis and insulin resistance by the plasma membrane sn-1,2-DAGs–PKCε–insulin receptor kinaseT1150 pathway
Zheng J, Gaspar R, Sakuma I, Hubbard B, Zhang D, Nasiri A, Kahn M, Perelis M, Samuel V, Petersen K, Shulman G. Cideb knockdown in mice increases mitochondrial fat oxidation and reverses hepatic steatosis and insulin resistance by the plasma membrane sn-1,2-DAGs–PKCε–insulin receptor kinaseT1150 pathway. Diabetologia 2025, 68: 2906-2920. PMID: 40908405, DOI: 10.1007/s00125-025-06539-8.Peer-Reviewed Original ResearchCitationsAltmetricConceptsMitochondrial fat oxidationWhole-body energy expenditureTricarboxylic acidIn vivo rateHFD-induced hepatic steatosisHigh-fat dietHFD-induced insulin resistanceSteatotic liver diseaseAntisense oligonucleotidesHepatic lipogenesisHepatic mitochondrial oxidationHepatic insulin resistanceCidebHepatic steatosisComprehensive Lab Animal Monitoring SystemHigh-fat diet mouse modelInsulin resistanceMitochondrial oxidationMethodsC57BL/6J male miceRadio-labelled isotopesHyperinsulinaemic–euglycaemic clamp studiesKnockdownASO treatmentLipogenesisConclusions/interpretationThese findingsp53-inducible lncRNA LOC644656 causes genotoxic stress-induced stem cell maldifferentiation and cancer chemoresistance
Tamura A, Yamagata K, Kono T, Fujimoto M, Fuchigami T, Nishimura M, Yokoyama M, Nakayama A, Hashimoto N, Sakuma I, Mitsukawa N, Kawashima Y, Ohara O, Motohashi S, Kawakami E, Miki T, Onodera A, Tanaka T. p53-inducible lncRNA LOC644656 causes genotoxic stress-induced stem cell maldifferentiation and cancer chemoresistance. Nature Communications 2025, 16: 4818. PMID: 40410129, PMCID: PMC12102190, DOI: 10.1038/s41467-025-59886-w.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsDNA damage responseDamage responseDNA damageDNA damage signalingResistance to genotoxic stressTGF-b signalingGenotoxic stressDamage signalingDNA-PKcsLineage-specific differentiationLoss of stemnessPoor patient survivalStem cell biologyEmbryonic stem cellsMolecular mechanismsDNACell biologyEnhanced chemoresistanceCancer chemoresistancePotential therapeutic targetDifferentiation pathwayCell propagationHuman embryonic stem cellsStem cell propagationChemoresistanceLiver lipid droplet cholesterol content is a key determinant of metabolic dysfunction–associated steatohepatitis
Sakuma I, Gaspar R, Nasiri A, Dufour S, Kahn M, Zheng J, LaMoia T, Guerra M, Taki Y, Kawashima Y, Yimlamai D, Perelis M, Vatner D, Petersen K, Huttasch M, Knebel B, Kahl S, Roden M, Samuel V, Tanaka T, Shulman G. Liver lipid droplet cholesterol content is a key determinant of metabolic dysfunction–associated steatohepatitis. Proceedings Of The National Academy Of Sciences Of The United States Of America 2025, 122: e2502978122. PMID: 40310463, PMCID: PMC12067271, DOI: 10.1073/pnas.2502978122.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsCholine-deficient l-amino acid-defined high-fat dietBempedoic acidLiver fibrosisLiver diseaseL-amino acid-defined high-fat dietAdvanced liver diseaseCholesterol contentHSD17B13 variantsHigh-fat dietTotal liver cholesterol contentTreated miceActivate signaling pathwaysVariant rs738409Liver cholesterol contentLiver lipidsFibrotic responsePromote inflammationTherapeutic approachesSteatotic liver diseaseDietary cholesterol supplementationFibrosisHuman liver samplesI148MAntisense oligonucleotidesProgressive formProtocol for characterizing craniopharyngioma subtypes and their microenvironments using single-cell RNA sequencing and immunohistochemistry
Kono T, Matsuda T, Fujimoto M, Taki Y, Sakuma I, Hashimoto N, Nakamura Y, Horiguchi K, Higuchi Y, Onodera A, Miki T, Tanaka T. Protocol for characterizing craniopharyngioma subtypes and their microenvironments using single-cell RNA sequencing and immunohistochemistry. STAR Protocols 2025, 6: 103760. PMID: 40238632, PMCID: PMC12022695, DOI: 10.1016/j.xpro.2025.103760.Peer-Reviewed Original ResearchAltmetricMeSH Keywords and ConceptsShort- and long-term glycemic effects of pasireotide in patients with acromegaly: a comprehensive case study with review of literature
Taki Y, Kono T, Matsuda T, Kozu R, Fujimoto M, Sakuma I, Hashimoto N, Horiguchi K, Higuchi Y, Tanaka T. Short- and long-term glycemic effects of pasireotide in patients with acromegaly: a comprehensive case study with review of literature. Endocrine Journal 2025, 72: 421-435. PMID: 39842795, PMCID: PMC11997266, DOI: 10.1507/endocrj.ej24-0548.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsCitationsAltmetricConceptsSomatostatin receptor 5GLP-1RAsContinuous glucose monitoringGrowth hormoneOptimal first-line treatmentGLP-1 receptor agonistsEfficacy of GLP-1RAsMultireceptor somatostatin analogsEffects of pasireotideFirst-line therapyFirst-line treatmentInsulin-like growth factor-1Optimal treatment strategyControlling hormone levelsEarly detectionGrowth factor-1Pasireotide therapyInhibit insulin secretionSomatostatin analogsFirst-lineReceptor agonistsTreatment optionsPasireotideReceptor 5Treatment strategies
2024
Comparative analysis of aldosterone and renin assays for primary aldosteronism screening
Taki Y, Kono T, Teruyama K, Ichijo T, Sakuma I, Nagano H, Miyagawa H, Kono S, Fujimoto M, Hashimoto N, Yokoyama M, Kawakami E, Miki T, Tanaka T. Comparative analysis of aldosterone and renin assays for primary aldosteronism screening. Scientific Reports 2024, 14: 26040. PMID: 39472614, PMCID: PMC11522277, DOI: 10.1038/s41598-024-75645-1.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsAldosterone-to-renin ratioPlasma aldosterone concentrationWeak mineralocorticoidLC-MS/MSPrimary aldosteronismChemiluminescent enzyme immunoassayAnalysis of aldosteroneLiquid chromatography/mass spectrometry/mass spectrometryPA diagnosisPrimary aldosteronism screeningNon-PA groupPlasma aldosterone concentration valuesReceiver operating characteristic curveRenin samplingRenin valuesAldosterone concentrationRetrospective studyCutoff valuePassing-Bablok regressionPAC samplesRenin assayPAC measurementsRadioimmunoassay methodEnzyme immunoassayRadioimmunoassayDeciphering craniopharyngioma subtypes: Single-cell analysis of tumor microenvironment and immune networks
Matsuda T, Kono T, Taki Y, Sakuma I, Fujimoto M, Hashimoto N, Kawakami E, Fukuhara N, Nishioka H, Inoshita N, Yamada S, Nakamura Y, Horiguchi K, Miki T, Higuchi Y, Tanaka T. Deciphering craniopharyngioma subtypes: Single-cell analysis of tumor microenvironment and immune networks. IScience 2024, 27: 111068. PMID: 39483146, PMCID: PMC11525618, DOI: 10.1016/j.isci.2024.111068.Peer-Reviewed Original ResearchCitationsAltmetricConceptsTumor microenvironmentAnalysis of tumor microenvironmentImmune responseOccurrence of diabetes insipidusExpression of pro-inflammatory markersCell-cell interactionsPro-inflammatory markersComprehensive cell atlasM2 macrophage ratioSquamous papillaryDiabetes insipidusTumor cellsSingle cell RNA sequencingMacrophage ratioM1 macrophagesM2 macrophagesPituitary structureCell RNA sequencingCellular compositionSingle-cell clusteringCell typesDiverse cell typesTumorGene expression patternsMolecular characteristicsSmall molecule inhibition of glycogen synthase I reduces muscle glycogen content and improves biomarkers in a mouse model of Pompe disease
Gaspar R, Sakuma I, Nasiri A, Hubbard B, LaMoia T, Leitner B, Tep S, Xi Y, Green E, Ullman J, Petersen K, Shulman G. Small molecule inhibition of glycogen synthase I reduces muscle glycogen content and improves biomarkers in a mouse model of Pompe disease. AJP Endocrinology And Metabolism 2024, 327: e524-e532. PMID: 39171753, PMCID: PMC11482269, DOI: 10.1152/ajpendo.00175.2024.Peer-Reviewed Original ResearchCitationsConceptsGAA-KO miceMouse model of Pompe diseaseModel of Pompe diseasePompe diseaseMetabolic dysregulationRegular chowMouse modelSmall molecule inhibitionInsulin sensitivityReduced spontaneous activityGroups of male miceEnzyme acid alpha-glucosidaseProgressive muscle weaknessImprove metabolic dysregulationSynthase IWhole-body insulin sensitivityAcid alpha-glucosidaseImproved glucose toleranceIncreased AMPK phosphorylationWT miceAbnormal accumulation of glycogenGlycogen storage disorderMale miceSpontaneous activityImproved biomarkers
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