2025
Deuterium MRS for In Vivo Measurement of Lipogenesis in the Liver
Gursan A, de Graaf R, Thomas M, Prompers J, De Feyter H. Deuterium MRS for In Vivo Measurement of Lipogenesis in the Liver. NMR In Biomedicine 2025, 38: e70014. PMID: 39994887, DOI: 10.1002/nbm.70014.Peer-Reviewed Original ResearchConceptsH-MRSHepatic DNLMRS dataLiver tissueMeasurement of lipogenesisDietary interventionLiver lipidsHepatic de novo lipogenesisLow density lipoproteinDetection of deuteriumGold standard measureMetabolic diseasesIncreased hepatic DNLLiverDensity lipoproteinDrinking waterDeuterium labelingIn vivo measurementsNMR dataExcised liver tissueTissueDeuteriumMRSMethylene resonancesDeuterated waterProtein Tyrosine Phosphatases in Metabolism: A New Frontier for Therapeutics
Bennett A, Tiganis T. Protein Tyrosine Phosphatases in Metabolism: A New Frontier for Therapeutics. Annual Review Of Physiology 2025, 87: 301-324. PMID: 39531392, DOI: 10.1146/annurev-physiol-022724-105540.Peer-Reviewed Original ResearchProtein tyrosine phosphataseFunction of protein tyrosine phosphatasesActions of protein tyrosine kinasesTyrosine phosphorylation-dependent signalingTyrosine phosphataseType 2 diabetesPhosphorylation-dependent signalingPathophysiology of metabolic diseasesPrevalence of chronic metabolic disordersProtein tyrosine kinasesMetabolic disordersChronic metabolic disorderMetabolic homeostasisTyrosine kinaseIncreased prevalencePharmaceutical strategiesMetabolic diseasesGlucose metabolismMetabolismProteinBody weightObesityPhosphataseComplex interplayDisorders
2024
Rewiring of the glymphatic landscape in metabolic disorders
Chen B, Meseguer D, Lenck S, Thomas J, Schneeberger M. Rewiring of the glymphatic landscape in metabolic disorders. Trends In Endocrinology And Metabolism 2024 PMID: 39638721, DOI: 10.1016/j.tem.2024.11.005.Peer-Reviewed Original ResearchMetabolic dysfunctionNeurological disordersBlood-brain barrier leakageCerebral blood flow disruptionBlood flow disruptionGlymphatic systemTreatment strategiesCognitive declineRisk factorsMetabolic disordersNeurovascular uncouplingBarrier leakageGlymphatic clearance systemMetabolic diseasesDisordersObesityDysfunctionToxic and Metabolic Diseases of the CNS
Subramanian H, Mahajan A. Toxic and Metabolic Diseases of the CNS. What Radiology Residents Need To Know 2024, 231-244. DOI: 10.1007/978-3-031-55124-6_16.ChaptersCentral nervous systemMetabolic disordersBrain parenchymal involvementPredominant site of involvementSite of involvementNonspecific imaging appearancesDeep white matterParenchymal involvementDifferential diagnosisSpinal cordSevere casesImaging appearanceCerebral cortexCorpus callosumWhite matterMetabolic diseasesNervous systemPredominant siteToxic etiologyBasal gangliaSevere disordersDiagnosisDisordersImage patternsImage featuresThe glymphatic system as a nexus between obesity and neurological diseases
Chen B, Lenck S, Thomas J, Schneeberger M. The glymphatic system as a nexus between obesity and neurological diseases. Nature Reviews Endocrinology 2024, 21: 1-2. PMID: 39304738, PMCID: PMC11801375, DOI: 10.1038/s41574-024-01042-3.Peer-Reviewed Original ResearchHuman AKR1C3 binds agonists of GPR84 and participates in an expanded polyamine pathway
Dudkina N, Park H, Song D, Jain A, Khan S, Flavell R, Johnson C, Palm N, Crawford J. Human AKR1C3 binds agonists of GPR84 and participates in an expanded polyamine pathway. Cell Chemical Biology 2024, 32: 126-144.e18. PMID: 39163853, PMCID: PMC11748234, DOI: 10.1016/j.chembiol.2024.07.011.Peer-Reviewed Original ResearchHuman aldo-keto reductase family 1 member C3Mammalian fatty acid synthaseDNA double-strand break responseDouble-strand break responseAldo-keto reductase family 1 member C3Associated with poor prognosisPolyamine pathwayFatty acid synthesisFatty acid synthaseAcid synthaseAKR1C3 activityPoor prognosisBiochemical roleAcid synthesisClinical significanceLigand screeningFerroptosis resistanceDNA damageAKR1C3Metabolic diseasesDiverse cancersDNANADPHAgonists of GPR84GPR84Modeling Glucose, Insulin, C-Peptide, and Lactate Interplay in Adolescents During an Oral Glucose Tolerance Test.
Bonet J, Barbieri E, Santoro N, Dalla Man C. Modeling Glucose, Insulin, C-Peptide, and Lactate Interplay in Adolescents During an Oral Glucose Tolerance Test. Journal Of Diabetes Science And Technology 2024, 19322968241266825. PMID: 39076151, PMCID: PMC11572107, DOI: 10.1177/19322968241266825.Peer-Reviewed Original ResearchOral glucose tolerance testArea under the curveGlucose tolerance testC-peptideTolerance testStandard oral glucose tolerance testPathological conditionsTime coursePopulation of adolescentsClinical dataLactate metabolism pathwaysLiver diseaseSteatotic liver diseaseModel glucoseMetabolic diseasesIntersubject variabilityObesityLactate metabolismAnaerobic glycolysisInsulinLactate kineticsDiseaseAdolescentsLactateMetabolic pathwaysWhite adipocytes in subcutaneous fat depots require KLF15 for maintenance in preclinical models
Li L, Feldman B. White adipocytes in subcutaneous fat depots require KLF15 for maintenance in preclinical models. Journal Of Clinical Investigation 2024, 134: e172360. PMID: 38949025, PMCID: PMC11213504, DOI: 10.1172/jci172360.Peer-Reviewed Original ResearchConceptsWhite adipose tissueSubcutaneous white adipose tissueBrown adipose tissueDeletion of KLF15Transcription factor KLF15Visceral white adipose tissueHuman adipose cellsWhite adipocytesAdipose tissueMolecular mechanismsKLF15Adipose cellsDepot-specificAdipocytesNormal physiologySubcutaneous fat depotsCell-specific propertiesAdipose tissue depotsHealthy adipose tissueDirectional regulationMetabolic diseasesDevelopment of therapiesPathwayCellsMouse modelDCRM 2.0: Multispecialty practice recommendations for the management of diabetes, cardiorenal, and metabolic diseases
Handelsman Y, Anderson J, Bakris G, Ballantyne C, Bhatt D, Bloomgarden Z, Bozkurt B, Budoff M, Butler J, Cherney D, DeFronzo R, Del Prato S, Eckel R, Filippatos G, Fonarow G, Fonseca V, Garvey W, Giorgino F, Grant P, Green J, Greene S, Groop P, Grunberger G, Jastreboff A, Jellinger P, Khunti K, Klein S, Kosiborod M, Kushner P, Leiter L, Lepor N, Mantzoros C, Mathieu C, Mende C, Michos E, Morales J, Plutzky J, Pratley R, Ray K, Rossing P, Sattar N, Schwarz P, Standl E, Steg P, Tokgözoğlu L, Tuomilehto J, Umpierrez G, Valensi P, Weir M, Wilding J, Wright E. DCRM 2.0: Multispecialty practice recommendations for the management of diabetes, cardiorenal, and metabolic diseases. Metabolism 2024, 159: 155931. PMID: 38852020, DOI: 10.1016/j.metabol.2024.155931.Peer-Reviewed Original ResearchChronic kidney diseaseAtherosclerotic cardiovascular diseaseHeart failureMetabolic diseasesCardiorenal risk factorsEssentials of managementPractice recommendationsType 2 diabetesImprove patient outcomesVolunteer task forcePrimary care physiciansMetabolic comorbiditiesMultispecialty consensusOutcome trialsManagement of personsKidney diseaseLiver diseasePathophysiological pathwaysPulmonary diseaseRisk factorsSteatotic liver diseaseManagement of diabetesCardiovascular diseasePatient outcomesCare physiciansEffects of gut microbiome on type 1 diabetes susceptibility and complications: A large‐scale bidirectional Mendelian randomization and external validation study
Guo K, Ye J, Li J, Huang J, Zhou Z. Effects of gut microbiome on type 1 diabetes susceptibility and complications: A large‐scale bidirectional Mendelian randomization and external validation study. Diabetes Obesity And Metabolism 2024, 26: 3306-3317. PMID: 38751358, DOI: 10.1111/dom.15658.Peer-Reviewed Original ResearchHigh-density lipoproteinOphthalmic complicationsT1D complicationsComplications of type 1 diabetesType 1 diabetes susceptibilityData of patientsRisk of T1DSmall high-density lipoproteinGut microbiomeComplications of T1DType 1 diabetesEffect of gut microbiomeExternal validation studyEffects of gut microbiotaCirculating metabolitesMultivariable MR analysisHealthy controlsComplicationsMR analysisMendelian randomizationRelative abundanceEubacterium coprostanoligenes groupMetabolic diseasesT1DPatientsAdiposity, immunity, and inflammation: interrelationships in health and disease: a report from 24th Annual Harvard Nutrition Obesity Symposium, June 2023
Burak M, Stanley T, Lawson E, Campbell S, Lynch L, Hasty A, Domingos A, Dixit V, Hotamışlıgil G, Sheedy F, Dixon A, Brinkley T, Hill J, Donath M, Grinspoon S. Adiposity, immunity, and inflammation: interrelationships in health and disease: a report from 24th Annual Harvard Nutrition Obesity Symposium, June 2023. American Journal Of Clinical Nutrition 2024, 120: 257-268. PMID: 38705359, PMCID: PMC11347817, DOI: 10.1016/j.ajcnut.2024.04.029.Peer-Reviewed Original ResearchLow-grade systemic inflammationChronic low-grade inflammationLocal immune environmentAdipose tissueLow-grade inflammationEffect of obesityObesity Research CenterPro-inflammatory pathwaysOutcome of metabolic diseasesImmune environmentSystemic inflammationHealth and DiseaseTreatment therapiesInflammationMultifaceted effectsDisease severityMetabolic diseasesImmunometabolic diseasesImmunityAdiposeDiseaseReduced disease severityObesityTissueDisrupting cellular homeostasisLongitudinal profiling of the microbiome at four body sites reveals core stability and individualized dynamics during health and disease
Zhou X, Shen X, Johnson J, Spakowicz D, Agnello M, Zhou W, Avina M, Honkala A, Chleilat F, Chen S, Cha K, Leopold S, Zhu C, Chen L, Lyu L, Hornburg D, Wu S, Zhang X, Jiang C, Jiang L, Jiang L, Jian R, Brooks A, Wang M, Contrepois K, Gao P, Rose S, Tran T, Nguyen H, Celli A, Hong B, Bautista E, Dorsett Y, Kavathas P, Zhou Y, Sodergren E, Weinstock G, Snyder M. Longitudinal profiling of the microbiome at four body sites reveals core stability and individualized dynamics during health and disease. Cell Host & Microbe 2024, 32: 506-526.e9. PMID: 38479397, PMCID: PMC11022754, DOI: 10.1016/j.chom.2024.02.012.Peer-Reviewed Original ResearchHost healthMicrobiome dynamicsBacterial taxaBody sitesMicrobiome stabilityIndividual taxaHuman microbiomeMicrobial compositionMicrobial dynamicsMulti-omicsNasal microbiomeMicrobiomeDisrupt interactionsMolecular markersBody-sitesTaxaHostMetabolic diseasesOral microbiomeInsulin-resistant individualsIndividual-specificTemporal dynamicsClinical featuresComprehensive viewClinical markersmicroRNA-33 controls hunger signaling in hypothalamic AgRP neurons
Price N, Fernández-Tussy P, Varela L, Cardelo M, Shanabrough M, Aryal B, de Cabo R, Suárez Y, Horvath T, Fernández-Hernando C. microRNA-33 controls hunger signaling in hypothalamic AgRP neurons. Nature Communications 2024, 15: 2131. PMID: 38459068, PMCID: PMC10923783, DOI: 10.1038/s41467-024-46427-0.Peer-Reviewed Original ResearchConceptsAgRP neuronsFeeding behaviorFatty acid metabolismNon-coding RNAsMitochondrial biogenesisRegulatory pathwaysTarget genesHypothalamic AgRP neuronsExcessive nutrient intakeCentral regulatorBioenergetic processesAcid metabolismActivation of AgRP neuronsModulate feeding behaviorCentral regulation of feeding behaviorRegulation of feeding behaviorMiR-33Hunger signalsMicroRNA-33Metabolic diseasesAlternative therapeutic approachLoss of miR-33Mouse modelMetabolic dysfunctionRegulation
2023
Association of Maternal Age and Blood Markers for Metabolic Disease in Newborns
Xie Y, Peng G, Zhao H, Scharfe C. Association of Maternal Age and Blood Markers for Metabolic Disease in Newborns. Metabolites 2023, 14: 5. PMID: 38276295, PMCID: PMC10821442, DOI: 10.3390/metabo14010005.Peer-Reviewed Original ResearchMaternal ageAdvanced maternal ageBlood metabolic markersMaternal age groupsInborn metabolic disordersNeonatal outcomesSingleton infantsGestational ageClinical variablesMarker levelsBirth weightBlood levelsBlood markersRisk factorsAge-related differencesInfant sexMetabolic disordersMetabolic markersPotential confoundingMetabolic diseasesScreening markerAge groupsBlood collectionScreening panelHigh false positive rateAdverse effects of gestational diabetes mellitus on fetal monocytes revealed by single-cell RNA sequencing
Yin M, Zhang Y, Li X, Liu S, Huang J, Yu H, Li X. Adverse effects of gestational diabetes mellitus on fetal monocytes revealed by single-cell RNA sequencing. IScience 2023, 27: 108637. PMID: 38188508, PMCID: PMC10770529, DOI: 10.1016/j.isci.2023.108637.Peer-Reviewed Original ResearchGestational diabetes mellitusCord blood mononuclear cellsBlood mononuclear cellsGDM mothersDiabetes mellitusMononuclear cellsCord bloodFetal monocytesMyeloid cellsMaternal gestational diabetes mellitusPeripheral blood mononuclear cellsAtherosclerotic cardiovascular diseasePrevalent metabolic disorderLong-term riskProliferation-related pathwaysCardiovascular diseaseMetabolic disordersNeutrophil granulocytesMetabolic diseasesSingle-cell RNA sequencingMonocytesPhagocytic abilityAdverse effectsPotential mechanismsMellitusHepatocyte CYR61 polarizes profibrotic macrophages to orchestrate NASH fibrosis
Mooring M, Yeung G, Luukkonen P, Liu S, Akbar M, Zhang G, Balogun O, Yu X, Mo R, Nejak-Bowen K, Poyurovsky M, Booth C, Konnikova L, Shulman G, Yimlamai D. Hepatocyte CYR61 polarizes profibrotic macrophages to orchestrate NASH fibrosis. Science Translational Medicine 2023, 15: eade3157. PMID: 37756381, PMCID: PMC10874639, DOI: 10.1126/scitranslmed.ade3157.Peer-Reviewed Original ResearchConceptsNonalcoholic steatohepatitisLiver inflammationNonalcoholic fatty liver diseaseProgression of NASHCysteine-rich angiogenic inducer 61Fatty liver diseaseLiver-specific knockout miceImproved glucose toleranceType 2 diabetesGlucose toleranceLiver diseaseNASH progressionProfibrotic macrophagesProinflammatory propertiesReduced fibrosisCardiovascular diseaseProfibrotic phenotypeFibrotic developmentKnockout miceNF-κBMetabolic diseasesNASH dietPDGFB expressionFibrosisProfibrotic programPrenatal Choline Supplement in a Maternal Obesity Model Modulates Offspring Hepatic Lipidomes
Korsmo H, Kadam I, Reaz A, Bretter R, Saxena A, Johnson C, Caviglia J, Jiang X. Prenatal Choline Supplement in a Maternal Obesity Model Modulates Offspring Hepatic Lipidomes. Nutrients 2023, 15: 965. PMID: 36839327, PMCID: PMC9963284, DOI: 10.3390/nu15040965.Peer-Reviewed Original ResearchConceptsMetabolic-associated fatty liver diseaseMaternal choline supplementationHF feedingHepatic lipidomeCholine supplementationMale offspringFatty liver diseaseChronic metabolic diseaseSemi-essential nutrientsNervonic acidEmbryonic day 17.5MAFLD progressionMaternal obesityLiver diseaseInsulin resistanceMouse offspringObesogenic dietOffspring liverLipid overloadOffspring healthLower oxidative stressMetabolic diseasesCholine supplementsMacronutrient metabolismDay 17.5Mitogen-Activated Protein Kinase Phosphatases: No Longer Undruggable?
Shillingford S, Bennett A. Mitogen-Activated Protein Kinase Phosphatases: No Longer Undruggable? The Annual Review Of Pharmacology And Toxicology 2023, 63: 617-636. PMID: 36662585, PMCID: PMC10127142, DOI: 10.1146/annurev-pharmtox-051921-121923.Peer-Reviewed Original ResearchConceptsMitogen-activated protein kinaseSmall molecule inhibitionProtein kinaseCritical cellular functionsInhibition of PTPsProtein tyrosineCellular functionsProtein substratesPhosphorylated proteinsCell signalingTyrosine residuesAttractive therapeutic targetCellular effectsKinaseNumerous diseasesPTPDiscovery toolTherapeutic developmentTherapeutic targetMetabolic diseasesInhibitionDephosphorylationSignalingMKPProtein
2022
Hospital admission risks and ambient fine particulate matter exposure in Beijing, China
Wu Z, Liang F, Chen X, Liu G, Li G, Tian L, Guo Q, Yang C, Zhou Z, Pan X, Liu Y. Hospital admission risks and ambient fine particulate matter exposure in Beijing, China. Atmospheric Environment 2022, 288: 119291. DOI: 10.1016/j.atmosenv.2022.119291.Peer-Reviewed Original ResearchHospital admission riskMalignant tumorsRespiratory diseaseAllergic diseasesUrogenital diseasesPM2.5 exposureMetabolic diseasesMental disordersAdmission riskLong-term exposureAmbient fine particulate matter (PM2.5) exposureFine particulate matter exposureAmbient PM2.5 exposureLong-term PM2.5 exposureParticulate matter exposurePoisson regression modelsAmbient PM2.5 levelsIschemic strokeCirculatory diseasesMatter exposureHA riskAge groupsTumorsDiseaseSubgroup populationsDownregulation 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 activityAMPKAblationDeficiencyCatabolismLKB1Hepatotoxicity
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