2023
Weight Loss-Independent Effect of Liraglutide on Insulin Sensitivity in Individuals With Obesity and Prediabetes.
Mashayekhi M, Nian H, Mayfield D, Devin J, Gamboa J, Yu C, Silver H, Niswender K, Luther J, Brown N. Weight Loss-Independent Effect of Liraglutide on Insulin Sensitivity in Individuals With Obesity and Prediabetes. Diabetes 2023, 73: 38-50. PMID: 37874653, PMCID: PMC10784656, DOI: 10.2337/db23-0356.Peer-Reviewed Original ResearchConceptsEndogenous GLP-1Glucagon-like peptide-1 receptor agonistsPeptide-1 receptor agonistsImproved insulin sensitivityInsulin sensitivityGLP-1GLP-1RGlucagon levelsGlucose levelsMatsuda indexWeight lossHypocaloric dietPostprandial glucoseInhibitor sitagliptinReceptor agonistMetabolic effectsDiet-induced weight lossDipeptidyl peptidase-4 inhibitor sitagliptinGLP-1R agonist liraglutideWeight loss-independent effectsDPP-4 inhibitor sitagliptinDipeptidyl peptidase-4 inhibitionPeptidase-4 inhibitionMixed meal testGLP-1R antagonist
2022
DPP4 (Dipeptidyl Peptidase-4) Inhibition Increases Catecholamines Without Increasing Blood Pressure During Sustained ACE (Angiotensin-Converting Enzyme) Inhibitor Treatment
Wilson JR, Garner EM, Mashayekhi M, Hubers SA, Bustamante C, Kerman SJ, Nian H, Shibao CA, Brown NJ. DPP4 (Dipeptidyl Peptidase-4) Inhibition Increases Catecholamines Without Increasing Blood Pressure During Sustained ACE (Angiotensin-Converting Enzyme) Inhibitor Treatment. Hypertension 2022, 79: 827-835. PMID: 35045722, PMCID: PMC8917054, DOI: 10.1161/hypertensionaha.121.18348.Peer-Reviewed Original ResearchMeSH KeywordsAdultAngiotensin Receptor AntagonistsAngiotensin-Converting Enzyme InhibitorsAngiotensinsAprepitantBlood PressureCardiovascular AgentsCatecholaminesCross-Over StudiesDiabetes Mellitus, Type 2Dipeptidyl Peptidase 4HumansNorepinephrineRamiprilRenin-Angiotensin SystemSitagliptin PhosphateValsartanConceptsDPP4 inhibitionBlood pressureACE inhibitionDouble-blind crossover studyAcute ACE inhibitionBlood pressure armNK1 receptor blockerACE inhibitor treatmentOral diabetes medicationsCalcium channel blockersType 2 diabetesEffects of DPP4Aldosterone systemCardiovascular complicationsDiabetes medicationsReceptor blockersCardiovascular effectsCrossover therapyHeart failureHypotensive effectCrossover studyChannel blockersDPP4 inhibitorsHeart rateInhibitor treatment
2021
GSK2256294 Decreases sEH (Soluble Epoxide Hydrolase) Activity in Plasma, Muscle, and Adipose and Reduces F2-Isoprostanes but Does Not Alter Insulin Sensitivity in Humans
Luther JM, Ray J, Wei D, Koethe JR, Hannah L, DeMatteo A, Manning R, Terker AS, Peng D, Nian H, Yu C, Mashayekhi M, Gamboa J, Brown NJ. GSK2256294 Decreases sEH (Soluble Epoxide Hydrolase) Activity in Plasma, Muscle, and Adipose and Reduces F2-Isoprostanes but Does Not Alter Insulin Sensitivity in Humans. Hypertension 2021, 78: 1092-1102. PMID: 34455816, PMCID: PMC8429121, DOI: 10.1161/hypertensionaha.121.17659.Peer-Reviewed Original Research
2019
Sitagliptin Decreases Visceral Fat and Blood Glucose in Women With Polycystic Ovarian Syndrome
Devin JK, Nian H, Celedonio JE, Wright P, Brown NJ. Sitagliptin Decreases Visceral Fat and Blood Glucose in Women With Polycystic Ovarian Syndrome. The Journal Of Clinical Endocrinology & Metabolism 2019, 105: dgz028. PMID: 31529097, PMCID: PMC7947776, DOI: 10.1210/clinem/dgz028.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultBiomarkersBlood GlucoseCross-Over StudiesDipeptidyl Peptidase 4Dipeptidyl-Peptidase IV InhibitorsDouble-Blind MethodFemaleFollow-Up StudiesGlucose Tolerance TestHuman Growth HormoneHumansIntra-Abdominal FatMiddle AgedPolycystic Ovary SyndromePrognosisSitagliptin PhosphateYoung AdultConceptsOral glucose tolerance testPolycystic ovarian syndromeVisceral adiposityVascular functionGrowth hormoneOvarian syndromeGH secretionGlucagon-like peptide-1Increased visceral adiposityMaximal glucose responseOvernight GH secretionOvernight growth hormoneEarly insulin secretionGlucose tolerance testVenous samplingCrossover studyVisceral fatCrossover treatmentTolerance testBlood glucoseDPP4 inhibitionInsulin secretionPeak glucoseGlucose levelsPeptide-1
2018
Aprepitant for the Treatment of Pruritus in Sézary Syndrome: A Randomized Crossover Clinical Trial
Zic JA, Straka BT, McGirt LY, Nian H, Yu C, Brown NJ. Aprepitant for the Treatment of Pruritus in Sézary Syndrome: A Randomized Crossover Clinical Trial. JAMA Dermatology 2018, 154: 1221-1222. PMID: 30140912, PMCID: PMC6233739, DOI: 10.1001/jamadermatol.2018.2510.Peer-Reviewed Original ResearchDPP (Dipeptidyl Peptidase)-4 Inhibition Potentiates the Vasoconstrictor Response to NPY (Neuropeptide Y) in Humans During Renin-Angiotensin-Aldosterone System Inhibition
Hubers SA, Wilson JR, Yu C, Nian H, Grouzmann E, Eugster P, Shibao CA, Billings FT, Jafarian Kerman S, Brown NJ. DPP (Dipeptidyl Peptidase)-4 Inhibition Potentiates the Vasoconstrictor Response to NPY (Neuropeptide Y) in Humans During Renin-Angiotensin-Aldosterone System Inhibition. Hypertension 2018, 72: 712-719. PMID: 29987109, PMCID: PMC6202157, DOI: 10.1161/hypertensionaha.118.11498.Peer-Reviewed Original ResearchConceptsNPY infusionPlacebo-controlled crossover studyAngiotensin-converting enzyme inhibitorAldosterone system inhibitionDose-dependent vasoconstrictionIntra-arterial enalaprilatAngiotensin receptor blockersForearm blood flowHigh-risk patientsOrder of treatmentReceptor blockersVasoconstrictor effectVasoconstrictor responsesCardiovascular effectsRenin-AngiotensinBrachial arteryHeart failureNorepinephrine releaseCrossover studyEndogenous NPYY1 receptorCrossover treatmentSystem inhibitionY2 receptorsDPP4 inhibitionDipeptidyl Peptidase‐4 Inhibition Potentiates Stimulated Growth Hormone Secretion and Vasodilation in Women
Wilson JR, Brown NJ, Nian H, Yu C, Bidlingmaier M, Devin JK. Dipeptidyl Peptidase‐4 Inhibition Potentiates Stimulated Growth Hormone Secretion and Vasodilation in Women. Journal Of The American Heart Association 2018, 7: e008000. PMID: 29478970, PMCID: PMC5866333, DOI: 10.1161/jaha.117.008000.Peer-Reviewed Original ResearchMeSH KeywordsAdministration, OralAdultCross-Over StudiesDipeptidyl Peptidase 4Dipeptidyl-Peptidase IV InhibitorsDouble-Blind MethodFemaleFibrinolysisHuman Growth HormoneHumansInsulin-Like Growth Factor IMaleSecretory PathwaySex FactorsSitagliptin PhosphateTime FactorsTissue Plasminogen ActivatorUp-RegulationVasodilationYoung AdultConceptsFree insulin-like growth factor-1Insulin-like growth factor-1Growth factor-1GH secretionGrowth hormoneGHR blockadeVascular resistanceFactor 1Nitric oxideTissue plasminogen activator activityPeptidase-4 inhibitionImpaired endothelial functionGrowth hormone secretionReceptor-dependent effectsDipeptidyl peptidase-4Study drugEndothelial functionPlasminogen activator activityCrossover studyHormone secretionPeptidase-4VasodilationHealthy adultsGH receptorInhibition potentiates
2015
Angiotensin converting enzyme inhibition increases ADMA concentration in patients on maintenance hemodialysis – a randomized cross-over study
Gamboa JL, Pretorius M, Sprinkel KC, Brown NJ, Ikizler TA. Angiotensin converting enzyme inhibition increases ADMA concentration in patients on maintenance hemodialysis – a randomized cross-over study. BMC Nephrology 2015, 16: 167. PMID: 26494370, PMCID: PMC4618919, DOI: 10.1186/s12882-015-0162-x.Peer-Reviewed Original ResearchConceptsEnd-stage renal diseaseAngiotensin receptor blockersMaintenance hemodialysisCross-over studyADMA levelsAsymmetric dimethylarginineACE inhibitionADMA productionADMA concentrationsShort-term ACE inhibitionRandomized cross-over studyIntracellular ADMA concentrationStudy of patientsEffect of bradykininB2 receptor stimulationACE inhibitor-induced increaseInhibitor-induced increaseRamipril treatmentCardiovascular morbidityReceptor blockersEndothelial dysfunctionRenal diseaseBradykinin levelsBackgroundEndothelial dysfunctionDialysis session
2014
Dipeptidyl‐Peptidase 4 Inhibition and the Vascular Effects of Glucagon‐like Peptide‐1 and Brain Natriuretic Peptide in the Human Forearm
Devin JK, Pretorius M, Nian H, Yu C, Billings FT, Brown NJ. Dipeptidyl‐Peptidase 4 Inhibition and the Vascular Effects of Glucagon‐like Peptide‐1 and Brain Natriuretic Peptide in the Human Forearm. Journal Of The American Heart Association 2014, 3: e001075. PMID: 25158865, PMCID: PMC4310400, DOI: 10.1161/jaha.114.001075.Peer-Reviewed Original ResearchConceptsGlucagon-like peptide-1Brain natriuretic peptideForearm blood flowNatriuretic peptideDPP4 inhibitionBlood flowPeptide-1Placebo-controlled crossover studyDipeptidyl peptidase-4 inhibitorsDipeptidyl peptidase-4 inhibitionForearm vascular resistanceDose-dependent vasodilationMean arterial pressureGLP-1 concentrationsHuman forearmSitagliptin useDirect vasodilatorVascular resistanceVasodilator responseVascular effectsArterial pressureBrachial arteryDiabetes mellitusGlycemic controlNorepinephrine releaseDietary Sodium Restriction Decreases Insulin Secretion Without Affecting Insulin Sensitivity in Humans
Luther JM, Byrne LM, Yu C, Wang TJ, Brown NJ. Dietary Sodium Restriction Decreases Insulin Secretion Without Affecting Insulin Sensitivity in Humans. The Journal Of Clinical Endocrinology & Metabolism 2014, 99: e1895-e1902. PMID: 25029426, PMCID: PMC4184066, DOI: 10.1210/jc.2014-2122.Peer-Reviewed Original ResearchConceptsHigh sodium dietHigh sodium intakeInsulin sensitivity indexSodium intakeInsulin secretionAldosterone systemAldosterone infusionInsulin sensitivityAcademic clinical research centerAcute insulin secretory responseLow dietary sodium intakeDecrease insulin secretionC-peptide responsePlasma renin activityDietary sodium intakeLow sodium dietSystolic blood pressureClinical Research CenterInsulin secretory responseAcute insulin responseHigh-risk individualsImpairs insulin secretionGlucose-stimulated insulinIncident diabetesNormotensive volunteersSubstance P Increases Sympathetic Activity During Combined Angiotensin-Converting Enzyme and Dipeptidyl Peptidase-4 Inhibition
Devin JK, Pretorius M, Nian H, Yu C, Billings FT, Brown NJ. Substance P Increases Sympathetic Activity During Combined Angiotensin-Converting Enzyme and Dipeptidyl Peptidase-4 Inhibition. Hypertension 2014, 63: 951-957. PMID: 24516103, PMCID: PMC3984385, DOI: 10.1161/hypertensionaha.113.02767.Peer-Reviewed Original ResearchMeSH KeywordsAdultAngiotensin-Converting Enzyme InhibitorsBlood PressureBradykininCross-Over StudiesDipeptidyl Peptidase 4Double-Blind MethodEnalaprilatEnzyme InhibitorsFemaleHeart RateHumansMaleMiddle AgedNeurotransmitter AgentsNorepinephrinePeptidyl-Dipeptidase APyrazinesSitagliptin PhosphateSubstance PSympathetic Nervous SystemTriazolesVascular ResistanceConceptsDipeptidyl peptidase-4 inhibitionPeptidase-4 inhibitionTissue plasminogen activator releaseSubstance PDipeptidyl peptidase-4Plasminogen activator releaseSympathetic activityPeptidase-4Activator releasePlacebo-controlled crossover studyDipeptidyl peptidase-4 inhibitorsType 2 diabetes mellitusIntra-arterial enalaprilatForearm vascular resistanceForearm blood flowMean arterial pressurePeptidase-4 inhibitorsAngiotensin converting enzymeSubstrates of angiotensinVascular resistanceVasodilator responseArterial pressureBrachial arteryDiabetes mellitusCrossover study
2013
Fenofibrate lowers blood pressure in salt-sensitive but not salt-resistant hypertension
Gilbert K, Nian H, Yu C, Luther JM, Brown NJ. Fenofibrate lowers blood pressure in salt-sensitive but not salt-resistant hypertension. Journal Of Hypertension 2013, 31: 820-829. PMID: 23385647, PMCID: PMC3800119, DOI: 10.1097/hjh.0b013e32835e8227.Peer-Reviewed Original ResearchConceptsBlood pressureSalt dietHeart ratePeroxisome proliferator-activated receptor α (PPARα) agonistSalt-resistant hypertensionPlasma renin activityRenal vascular resistanceEffect of fenofibrateLow-salt dietMean arterial pressureHigh-salt dietDouble-blind protocolTreatment of hyperlipidemiaReceptor α agonistSalt sensitivityHypertensive volunteersRenal vasoconstrictionRenin activitySodium excretionVascular resistanceArterial pressureHypertensive individualsSalt intakeSystolic pressureTreatment arms
2011
Comparative Effects of Angiotensin-Converting Enzyme Inhibition and Angiotensin-Receptor Blockade on Inflammation during Hemodialysis
Gamboa JL, Pretorius M, Todd-Tzanetos DR, Luther JM, Yu C, Ikizler TA, Brown NJ. Comparative Effects of Angiotensin-Converting Enzyme Inhibition and Angiotensin-Receptor Blockade on Inflammation during Hemodialysis. Journal Of The American Society Of Nephrology 2011, 23: 334-342. PMID: 22158433, PMCID: PMC3269170, DOI: 10.1681/asn.2011030287.Peer-Reviewed Original ResearchMeSH KeywordsAngiotensin Receptor AntagonistsAngiotensin-Converting Enzyme InhibitorsBlood CoagulationCD40 LigandCross-Over StudiesCytokinesDouble-Blind MethodFemaleHemodynamicsHumansInflammationKidney Failure, ChronicMaleMiddle AgedOxidative StressRamiprilRenal DialysisReninTetrazolesValineValsartanConceptsAngiotensin receptor blockersMaintenance hemodialysis patientsCardiovascular mortalityHemodialysis patientsACE inhibitorsGreater anti-inflammatory effectAngiotensin-Converting Enzyme InhibitionOxidative stressAngiotensin receptor blockadeIL-10 concentrationsD-dimer levelsIL-6 levelsProspective clinical trialsAnti-inflammatory effectsIL-1β concentrationsLevels of vWFSerial blood samplingCardiovascular eventsEndothelial dysfunctionCrossover studyWashout periodIsoprostane levelsClinical trialsDrug treatmentVWF levels
2009
Endogenous Bradykinin Contributes to Increased Plasminogen Activator Inhibitor 1 Antigen following Hemodialysis
Marney AM, Ma J, Luther JM, Ikizler TA, Brown NJ. Endogenous Bradykinin Contributes to Increased Plasminogen Activator Inhibitor 1 Antigen following Hemodialysis. Journal Of The American Society Of Nephrology 2009, 20: 2246-2252. PMID: 19628666, PMCID: PMC2754101, DOI: 10.1681/asn.2009050505.Peer-Reviewed Original ResearchConceptsPlasminogen activator inhibitor-1 antigenHoe 140Endogenous bradykininHemodialysis patientsMCP-1Receptor blocker HOE-140Placebo-controlled crossover studyOxidative stressChronic hemodialysis patientsMean arterial pressureCoronary artery diseaseKallikrein-kinin systemBradykinin receptor antagonismHeart rate responsePAI-1 antigenTissue plasminogen activatorEffect of dialysisEnd of dialysisProduction of bradykininInhibits platelet aggregationCardiovascular eventsHemodialysis populationArterial pressureArtery diseaseEndothelial releasePhosphodiesterase 5 Inhibition Improves β-Cell Function in Metabolic Syndrome
Hill KD, Eckhauser AW, Marney A, Brown NJ. Phosphodiesterase 5 Inhibition Improves β-Cell Function in Metabolic Syndrome. Diabetes Care 2009, 32: 857-859. PMID: 19196886, PMCID: PMC2671107, DOI: 10.2337/dc08-1862.Peer-Reviewed Original ResearchConceptsBeta-cell functionPhosphodiesterase-5 inhibitionMetabolic syndromeInsulin sensitivityPlasma renin activityDiastolic blood pressureΒ-cell functionRenin activityBlood pressureACE inhibitionAngiotensin IIFibrinolytic parametersACE activityGlucose homeostasisSeparate daysSyndromeRamiprilFibrinolysisTadalafilInhibitionTreatmentNovel strategyPlaceboResearch designWomen
2006
Bradykinin B2 Receptor Does Not Contribute to Blood Pressure Lowering during AT1 Receptor Blockade
LeFebvre J, Shintani A, Gebretsadik T, Petro JR, Murphey LJ, Brown NJ. Bradykinin B2 Receptor Does Not Contribute to Blood Pressure Lowering during AT1 Receptor Blockade. Journal Of Pharmacology And Experimental Therapeutics 2006, 320: 1261-1267. PMID: 17182977, DOI: 10.1124/jpet.106.117259.Peer-Reviewed Original ResearchConceptsPlasma renin activityHoe 140Endogenous bradykininReceptor blockadeBaseline plasma renin activityBlood pressure-lowering effectAT1 receptor blockadeSalt-depleted subjectsBlood pressure loweringBlood pressure responseEffect of angiotensinPressure-lowering effectAngiotensin I/Heart rate responseReceptor-independent mechanismD-Arg-ArgBradykinin B2 receptorPRA responseRenin activityChronic treatmentPlasma cGMPPressure loweringB2 receptorsEndocrine responsesHeart rateAngiotensin II Induces Interleukin-6 in Humans Through a Mineralocorticoid Receptor–Dependent Mechanism
Luther JM, Gainer JV, Murphey LJ, Yu C, Vaughan DE, Morrow JD, Brown NJ. Angiotensin II Induces Interleukin-6 in Humans Through a Mineralocorticoid Receptor–Dependent Mechanism. Hypertension 2006, 48: 1050-1057. PMID: 17043157, DOI: 10.1161/01.hyp.0000248135.97380.76.Peer-Reviewed Original ResearchConceptsMineralocorticoid receptor-dependent mechanismAngiotensin IIReceptor-dependent mechanismBlood pressureIL-6Normotensive subjectsCrossover studyHigh-sensitivity C-reactive proteinSerum IL-6 concentrationDouble-blind crossover studyOxidative stressWeeks of placeboIL-6 concentrationsC-reactive proteinRenal plasma flowIntravenous aldosteroneAldosterone responseSerum potassiumInterleukin-6Mineralocorticoid receptorPlaceboAldosteroneSpironolactoneSeparate daysReceptor independent
2005
Prevalence of primary hyperaldosteronism in mild to moderate hypertension without hypokalaemia
Williams JS, Williams GH, Raji A, Jeunemaitre X, Brown NJ, Hopkins PN, Conlin PR. Prevalence of primary hyperaldosteronism in mild to moderate hypertension without hypokalaemia. Journal Of Human Hypertension 2005, 20: 129-136. PMID: 16292348, DOI: 10.1038/sj.jhh.1001948.Peer-Reviewed Original ResearchConceptsHigh sodium dietPrimary hyperaldosteronismModerate hypertensionSodium restrictionHypertensive populationLow serum potassium levelsNormotensive control populationSerum potassium levelsHigh blood pressureSpecific cutoff valuesElevated AERElevated ARRHaemodynamic testingNormotensive populationResistant hypertensionHypertensive subjectsNormotensive subjectsSerum aldosteroneBlood pressureEssential hypertensivesMedication washoutStudy protocolHypokalaemiaCutoff valueControl populationMelanocortin-4 Receptor–Deficient Mice Are Not Hypertensive or Salt-Sensitive Despite Obesity, Hyperinsulinemia, and Hyperleptinemia
Ma J, Albornoz F, Yu C, Byrne DW, Vaughan DE, Brown NJ. Melanocortin-4 Receptor–Deficient Mice Are Not Hypertensive or Salt-Sensitive Despite Obesity, Hyperinsulinemia, and Hyperleptinemia. Hypertension 2005, 46: 326-332. PMID: 15998706, DOI: 10.1161/01.hyp.0000174327.53863.86.Peer-Reviewed Original ResearchMeSH KeywordsAdultCross-Over StudiesDiureticsDouble-Blind MethodElectrolytesFemaleFibrinolysisHemodynamicsHumansHydrochlorothiazideHypertensionMaleMiddle AgedMineralocorticoid Receptor AntagonistsPlasminogen Activator Inhibitor 1PotassiumReceptors, MineralocorticoidRenin-Angiotensin SystemSodium Chloride Symporter InhibitorsSpironolactoneTriamtereneConceptsPAI-1 antigenMineralocorticoid receptor antagonismHypertensive subjectsPAI-1 responseTissue-type plasminogen activatorAldosterone systemNormotensive subjectsFibrinolytic balanceReceptor antagonismMelanocortin 4 receptor-deficient micePlasminogen activator inhibitor-1 (PAI-1) concentrationsEffect of spironolactoneReceptor-deficient miceEffect of triamtereneBlood pressureSerum potassiumTreatment groupsEffects of activationSpironolactonePAI-1Plasminogen activatorAntigenTriamtereneRegression analysisSubjects
2002
Spironolactone Abolishes the Relationship between Aldosterone and Plasminogen Activator Inhibitor-1 in Humans
Sawathiparnich P, Kumar S, Vaughan DE, Brown NJ. Spironolactone Abolishes the Relationship between Aldosterone and Plasminogen Activator Inhibitor-1 in Humans. The Journal Of Clinical Endocrinology & Metabolism 2002, 87: 448-452. PMID: 11836266, DOI: 10.1210/jcem.87.2.7980.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAldosteroneAntihypertensive AgentsBlood PressureCross-Over StudiesDiureticsDouble-Blind MethodFibrinolysisHumansHydrochlorothiazideHypertensionMaleMiddle AgedMineralocorticoid Receptor AntagonistsPlasminogen Activator Inhibitor 1Sodium Chloride Symporter InhibitorsSpironolactoneConceptsPAI-1 antigenT-PA antigenAngiotensin IITissue-type plasminogen activator antigenEffect of spironolactoneSystolic blood pressureMale hypertensive subjectsPlasminogen activator antigenPlasminogen activator inhibitor-1Plasminogen activator inhibitor-1 productionActivator inhibitor-1PAI-1 productionAldosterone systemHypertensive subjectsSerum aldosteroneBlood pressureEndogenous aldosteroneHemodynamic parametersAldosteroneStudy daysSpironolactoneHCTZPAI-1AntigenInhibitor-1