Milo White, MD
Assistant Professor of NeurologyAbout
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Featured Publications
Mechanism of Insulin Action
White M. Mechanism of Insulin Action. 2024, 111-127. DOI: 10.1002/9781119697473.ch9.Peer-Reviewed Original ResearchReceptor tyrosine kinasesTyrosine kinaseGrowth factor signalingSecrete sufficient insulinDysregulated insulin signalingPancreatic beta cellsMuscle insulin resistanceEnvironmental signalsSignal transductionInsulin signalingMuscle-specific deletionSystemic insulin actionSystemic insulin resistanceAdequate insulin responseFactor signalingInsulin-like growth factor signalingPlasma membraneInsulin resistanceInsulin receptorLigand bindingBeta cellsMetabolic stressChronic insulin resistanceGlucose transportTransphosphorylationBRD7 improves glucose homeostasis independent of IRS proteins.
Kim Y, Lee J, Han Y, Tao R, White M, Liu R, Park S. BRD7 improves glucose homeostasis independent of IRS proteins. Journal Of Endocrinology 2023, 258 PMID: 37578842, PMCID: PMC10430774, DOI: 10.1530/joe-23-0119.Peer-Reviewed Original ResearchConceptsGlucose homeostasisKnockout miceAlternative insulinObese miceGlucose homeostasis independentGlucose metabolism parametersContext of obesityBlood glucose levelsMetabolism parametersGlucose levelsGlucose metabolismInsulinMiceIRS proteinsInsulin receptorProtein 7ObesityHomeostasisUpregulationBRD7InvolvementPathwayNovel insightsEuglycemiaFindings1632-P: Effects of MTOR Signaling in Muscle-Specific Irs1/2 Knockout Mice
STOEHR O, COPPS K, TAO R, WHITE M. 1632-P: Effects of MTOR Signaling in Muscle-Specific Irs1/2 Knockout Mice. Diabetes 2023, 72 DOI: 10.2337/db23-1632-p.Peer-Reviewed Original ResearchMTKO miceGlucose uptakeMTOR pathwayMdKO miceReduced ejection fractionCardiac fatty acid uptakeHigh-fat dietInsulin-resistant heartMuscle glucose uptakeDays of lifeWhite adipose tissueCardiac glucose uptakeFatty acid uptakeEffects of mTORInsulin-stimulated conditionsEjection fractionFat dietFat massMuscle atrophyIRS2 expressionCardiac hypertrophyEarly deathCardiac energyKnockout miceAdipose tissueHepatic follistatin increases basal metabolic rate and attenuates diet-induced obesity during hepatic insulin resistance
Tao R, Stöhr O, Wang C, Qiu W, Copps K, White M. Hepatic follistatin increases basal metabolic rate and attenuates diet-induced obesity during hepatic insulin resistance. Molecular Metabolism 2023, 71: 101703. PMID: 36906067, PMCID: PMC10033741, DOI: 10.1016/j.molmet.2023.101703.Peer-Reviewed Original ResearchConceptsHepatic insulin resistanceInsulin resistanceAdipose massBasal metabolic rateHepatic disruptionDiet-induced obesityFat mass accumulationTotal lean massHigh-fat dietBody weight changesHFD consumptionFat massLean massFOXO1-dependent mannerHepatic overexpressionHepatic insulinObesityMetabolic rateThe role of hepatokines in NAFLD
Stefan N, Schick F, Birkenfeld A, Häring H, White M. The role of hepatokines in NAFLD. Cell Metabolism 2023, 35: 236-252. PMID: 36754018, PMCID: PMC10157895, DOI: 10.1016/j.cmet.2023.01.006.Peer-Reviewed Original ResearchConceptsNon-alcoholic fatty liver diseaseNon-communicable diseasesInsulin resistanceVisceral obesityMajor non-communicable diseasesRole of hepatokinesFatty liver diseaseRole of fetuinVisceral adiposityFatty liverLiver diseaseCardiometabolic diseasesPathophysiological mechanismsOrgan crosstalkHepatokinesMain pathomechanismClinical practiceImportant causeDiseasePrecision medicineAdipokinesObesityMetabolismAdiposityPathomechanismLower Hepatic Fat Is Associated With Improved Insulin Secretion in a High-Risk Prediabetes Subphenotype During Lifestyle Intervention
Wagner R, Heni M, Kantartzis K, Sandforth A, Machann J, Schick F, Peter A, Fritsche L, Szendrödi J, Pfeiffer A, Schürmann A, Blüher M, Hauner H, Seissler J, Bornstein S, Roden M, Stefan N, Birkenfeld A, White M, Häring H, Fritsche A. Lower Hepatic Fat Is Associated With Improved Insulin Secretion in a High-Risk Prediabetes Subphenotype During Lifestyle Intervention. Diabetes 2022, 72: 362-366. PMID: 36525512, PMCID: PMC9935494, DOI: 10.2337/db22-0441.Peer-Reviewed Original ResearchConceptsInsulin secretionLifestyle interventionLiver fatOral glucose tolerance testHigh liver fatLifestyle intervention studyGlucose tolerance testHigh-risk clustersHepatic fatTolerance testInsulin sensitivitySpecific subphenotypesIntervention studiesSecretionTime pointsInterventionPrediabetesGlycemic traitsFatSubphenotypesGlycemiaCluster 3Downregulation of hepatic ceruloplasmin ameliorates NAFLD via SCO1-AMPK-LKB1 complex
Xie L, Yuan Y, Xu S, Lu S, Gu J, Wang Y, Wang Y, Zhang X, Chen S, Li J, Lu J, Sun H, Hu R, Piao H, Wang W, Wang C, Wang J, Li N, White M, Han L, Jia W, Miao J, Liu J. Downregulation of hepatic ceruloplasmin ameliorates NAFLD via SCO1-AMPK-LKB1 complex. Cell Reports 2022, 41: 111498. PMID: 36261001, PMCID: PMC10153649, DOI: 10.1016/j.celrep.2022.111498.Peer-Reviewed Original ResearchConceptsNon-alcoholic fatty liver diseaseFatty liver diseaseLipid metabolism diseasesLipid catabolismHepatic lipid catabolismFatty acid oxidationDetectable hepatotoxicityCopper deficiencyNAFLD developmentLiver diseaseMetabolic diseasesMetabolism diseasesNormal levelsDiseaseMitochondrial biogenesisAcid oxidationAMPK activityAMPKAblationDeficiencyCatabolismLKB1HepatotoxicityThe P300 acetyltransferase inhibitor C646 promotes membrane translocation of insulin receptor protein substrate and interaction with the insulin receptor
Peng J, Ramatchandirin B, Wang Y, Pearah A, Namachivayam K, Wolf R, Steele K, MohanKumar K, Yu L, Guo S, White M, Maheshwari A, He L. The P300 acetyltransferase inhibitor C646 promotes membrane translocation of insulin receptor protein substrate and interaction with the insulin receptor. Journal Of Biological Chemistry 2022, 298: 101621. PMID: 35074429, PMCID: PMC8850660, DOI: 10.1016/j.jbc.2022.101621.Peer-Reviewed Original ResearchConceptsAbsence of insulinP300 acetyltransferase activityTyrosine kinase activityAcetyltransferase activityInsulin receptorObese patientsTyrosine phosphorylationRole of acetylationInsulinNormal functionMembrane translocationSubsequent activationC646PatientsLiver hepatocytesProtein substratesInhibitionReceptorsMolecular mechanismsHepatocytesPhosphorylationBeta subunitKinase activityObesityUnique effectsElevated circulating follistatin associates with an increased risk of type 2 diabetes
Wu C, Borné Y, Gao R, López Rodriguez M, Roell W, Wilson J, Regmi A, Luan C, Aly D, Peter A, Machann J, Staiger H, Fritsche A, Birkenfeld A, Tao R, Wagner R, Canouil M, Hong M, Schwenk J, Ahlqvist E, Kaikkonen M, Nilsson P, Shore A, Khan F, Natali A, Melander O, Orho-Melander M, Nilsson J, Häring H, Renström E, Wollheim C, Engström G, Weng J, Pearson E, Franks P, White M, Duffin K, Vaag A, Laakso M, Stefan N, Groop L, De Marinis Y. Elevated circulating follistatin associates with an increased risk of type 2 diabetes. Nature Communications 2021, 12: 6486. PMID: 34759311, PMCID: PMC8580990, DOI: 10.1038/s41467-021-26536-w.Peer-Reviewed Original ResearchConceptsAdipose tissue insulin resistanceTissue insulin resistanceType 2 diabetesFollistatin levelsGlucokinase regulatory protein geneFollistatin secretionHazard ratioInsulin resistanceNon-alcoholic fatty liver diseaseAdjusted hazard ratioFatty liver diseaseRisk of T2DFree fatty acid releaseFatty acid releaseIncident T2DLiver diseaseGenome-wide association studiesHuman adipocytesT2DAcid releaseStandard deviation increaseDiabetesSecretionRiskRegulatory protein geneTAZ inhibits glucocorticoid receptor and coordinates hepatic glucose homeostasis in normal physiological states
Xu S, Liu Y, Hu R, Wang M, Stöhr O, Xiong Y, Chen L, Kang H, Zheng L, Cai S, He L, Wang C, Copps K, White M, Miao J. TAZ inhibits glucocorticoid receptor and coordinates hepatic glucose homeostasis in normal physiological states. ELife 2021, 10: e57462. PMID: 34622775, PMCID: PMC8555985, DOI: 10.7554/elife.57462.Peer-Reviewed Original ResearchConceptsGluconeogenic gene promotersBinding of GRGene promoterGlucocorticoid receptorGlucose homeostasisLigand-binding domainGlucose productionOverexpression of TAZHepatic glucose homeostasisWW domainsBlood glucose concentrationPhysiological fastingGluconeogenic genesGR response elementResponse elementNovel roleTAZNormal physiological stateGR transactivationPhysiological statePromoterMouse liverPericentral hepatocytesPathological statesGlucose concentration
Academic Achievements & Community Involvement
Clinical Care
Overview
Milo White, MD, is a neurologist who specializes in neurology and neurovascular surgery. He focuses on diagnosing and treating conditions such as stroke and language deficits related to autism.
As an assistant professor of neurology at Yale School of Medicine, Dr. White conducts research on pre-diabetes treatment in relation to stroke recurrence and explores brain anatomy related to speech and language issues in autism.
Dr. White earned his medical degree from the University of Utah School of Medicine.
Clinical Specialties
Neurology; Neurovascular Surgery
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