2025
1686-P: Novel Combination of a Mitochondrial Protonophore (MP) and an Acetyl-CoA Carboxylase 2 (ACC2) Inhibitor Causes Weight Loss and Preserves Lean Mass in Obese Mice
SRODA N, SHARMA M, MURAKAMI E, LOGAN C, WENG S, KIRBY B, MYERS R, SUBRAMANIAN M, SHULMAN G, VIJAYAKUMAR A. 1686-P: Novel Combination of a Mitochondrial Protonophore (MP) and an Acetyl-CoA Carboxylase 2 (ACC2) Inhibitor Causes Weight Loss and Preserves Lean Mass in Obese Mice. Diabetes 2025, 74 DOI: 10.2337/db25-1686-p.Peer-Reviewed Original ResearchLean massMitochondrial protonophoreDIO miceFood intakeFat mass lossReduced lean massWeight lossBody weightAcetyl-CoA carboxylase 2Obesity-associated disordersMale DIO miceFat massSemaglutideDiet-inducedNovel combinationObese miceMetabolic disordersEnhanced fatty acid oxidationMiceFatty acid oxidationEvaluation of combinationsObesityInhibitorsTreated withIntake1687-P: Sequential Combination of the Mitochondrial Protonophore (MP) TLC-6740 with Semaglutide Normalizes Body Weight and Preserves Lean Mass in DIO Mice
SRODA N, SHARMA M, MURAKAMI E, LOGAN C, WENG S, KIRBY B, MYERS R, SUBRAMANIAN M, SHULMAN G, VIJAYAKUMAR A. 1687-P: Sequential Combination of the Mitochondrial Protonophore (MP) TLC-6740 with Semaglutide Normalizes Body Weight and Preserves Lean Mass in DIO Mice. Diabetes 2025, 74 DOI: 10.2337/db25-1687-p.Peer-Reviewed Original ResearchLean massDIO miceFM lossBody weightMitochondrial protonophoreData support evaluationNormal body weightReduced food intakeRegulate body weightOral glucose toleranceEvaluate weight lossIncreased energy expenditureMale DIO miceSequential combinationDiet-inducedFood intakeGlucose toleranceMetabolic disordersSemaglutideMiceWeight lossEnergy expenditureOGTTOGTT AUCIncretin1694-P: De Novo or Sequential Combination of the Mitochondrial Protonophore TLC-1180 with Semaglutide Improves Weight Loss and Preserves Lean Mass in Dio Mice
SHARMA M, SRODA N, MURAKAMI E, LOGAN C, WENG S, KIRBY B, MYERS R, SUBRAMANIAN M, SHULMAN G, VIJAYAKUMAR A. 1694-P: De Novo or Sequential Combination of the Mitochondrial Protonophore TLC-1180 with Semaglutide Improves Weight Loss and Preserves Lean Mass in Dio Mice. Diabetes 2025, 74 DOI: 10.2337/db25-1694-p.Peer-Reviewed Original ResearchContraceptive Selection for the Endocrine Patient: What an Endocrinologist Should Know
Zaman A, Lazorwitz A, Wierman M. Contraceptive Selection for the Endocrine Patient: What an Endocrinologist Should Know. Endocrine Reviews 2025, bnaf016. PMID: 40519043, DOI: 10.1210/endrev/bnaf016.Peer-Reviewed Original ResearchContraceptive methodsPregnancy preventionSex steroid replacementHormonal contraceptive methodsHypothalamic-pituitary-gonadal axisBirth control optionsAndrogen suppressionRegular mensesSteroid replacementContraceptive optionsContraceptive usageContraceptive selectionEndocrine patientsEndocrine disordersMetabolic disordersContraceptionEndocrinologistsClinical practiceExogenous hormonesPregnancyPatientsHistory of contraceptionHormoneComprehensive careMedical providersCharacterization and lineage tracing of a mouse adipose depot reveal properties conserved with human supraclavicular brown adipose tissue
Li L, Feldman B. Characterization and lineage tracing of a mouse adipose depot reveal properties conserved with human supraclavicular brown adipose tissue. Stem Cell Reports 2025, 20: 102509. PMID: 40409261, PMCID: PMC12181967, DOI: 10.1016/j.stemcr.2025.102509.Peer-Reviewed Original ResearchConceptsInguinal white adipose tissueBrown adipose tissueSupraclavicular brown adipose tissuePreclinical modelsAdipose tissueActivation of beige adipocytesBeige adipose tissueAdipose tissue developmentWhite adipose tissueRobust preclinical modelsBeige fatDevelopmental originsMolecular markersSuccess of therapyTissue developmentThermogenic activityAdipose tissue depotsLineage tracingCell originLineagesAdipose depotsTherapeutic benefitMetabolic disordersTissue depotsMiceSuppression of endothelial ceramide de novo biosynthesis by Nogo-B contributes to cardiometabolic diseases
Rubinelli L, Manzo O, Sungho J, Del Gaudio I, Bareja R, Marino A, Palikhe S, Di Mauro V, Bucci M, Falcone D, Elemento O, Ersoy B, Diano S, Sasset L, Di Lorenzo A. Suppression of endothelial ceramide de novo biosynthesis by Nogo-B contributes to cardiometabolic diseases. Nature Communications 2025, 16: 1968. PMID: 40000621, PMCID: PMC11862206, DOI: 10.1038/s41467-025-56869-9.Peer-Reviewed Original ResearchConceptsNogo-BEndothelial dysfunctionHFD miceCardiometabolic diseasesSphingolipid signalingDevelopment of therapeutic strategiesBioactive sphingolipidsCeramide degradationSphingosine-1-phosphateHepatic glucose productionIn vivo evidenceEndothelial cellsEndothelial specific deletionCeramideBiosynthesisHigh-fat dietPathological implicationsSphingolipidsGlucose productionHFDIn vivoMale miceMetabolic dysfunctionTherapeutic strategiesMetabolic disordersA comprehensive spatio-cellular map of the human hypothalamus
Tadross J, Steuernagel L, Dowsett G, Kentistou K, Lundh S, Porniece M, Klemm P, Rainbow K, Hvid H, Kania K, Polex-Wolf J, Knudsen L, Pyke C, Perry J, Lam B, Brüning J, Yeo G. A comprehensive spatio-cellular map of the human hypothalamus. Nature 2025, 639: 708-716. PMID: 39910307, PMCID: PMC11922758, DOI: 10.1038/s41586-024-08504-8.Peer-Reviewed Original ResearchConceptsGenome-wide association study genesRare deleterious variantsHypothalamic cell typesCell typesSingle-nucleus sequencingBody mass indexTranscription mapDeleterious variantsNeuronal cell typesG protein-coupled receptorsStudy genesBiological functions1Spatial transcriptomicsTranscriptomic identityCellular componentsExpression levelsPro-opiomelanocortin neuronsHuman hypothalamusAssociated with body mass indexPopulation levelMetabolic disordersHypothalamic cellsExpressionNeuronal clustersTranscriptomeProtein 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, PMCID: PMC12134147, 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 featuresAssociation of uric acid and fructose levels in polycystic ovary syndrome
Feng D, Wang X, Song J, Yang H, Peng Y, Wang X, Chen W, Li P, Fang Y, Shi B, Li D. Association of uric acid and fructose levels in polycystic ovary syndrome. Human Reproduction 2024, 39: 2575-2586. PMID: 39380170, DOI: 10.1093/humrep/deae219.Peer-Reviewed Original ResearchPolycystic ovary syndromeSerum uric acidUric acid levelsSerum fructose levelsSerum uric acid levelsIndependent risk factorDiagnosis of polycystic ovary syndromeClinical diagnosis of polycystic ovary syndromeMetabolic disordersGranulosa cellsReal-time PCRControl womenShengjing HospitalMetabolic syndromeUric acidElevated serum uric acid levelsQuantitative real-time PCRRisk factorsAssociation of uric acidShengjing Hospital of China Medical UniversityAcid levelsInsulin resistanceIncreased risk of anovulationFructose metabolismHospital of China Medical UniversityAnalysis of drug–drug interactions in patients with HIV and metabolic syndrome
Tuan J, Igiraneza G, Ogbuagu O. Analysis of drug–drug interactions in patients with HIV and metabolic syndrome. Expert Opinion On Drug Metabolism & Toxicology 2024, 20: 953-965. PMID: 39230187, DOI: 10.1080/17425255.2024.2401044.Peer-Reviewed Original ResearchDrug-drug interactionsAntiretroviral therapyMetabolic disordersMetabolic syndromeNanotechnology-based drug delivery platformsPrevalence of metabolic comorbiditiesSelection of antiretroviral therapyLong-acting antiretroviral therapyContemporary antiretroviral therapyEffective antiretroviral therapyPrevalence of metabolic disordersRepertoire of treatment optionsDrug-drug interaction dataTreat metabolic syndromeMetabolic comorbiditiesTreatment optionsDrug delivery platformPrescribing informationAnalysis of drug-drug interactionsHIVInjectable medicationsDrug prescribing informationWeight lossPWHSyndromeObesity, Growth, Development, Metabolic Disorder, and Insulin Resistance in Pediatrics
Santoro N, Galderisi A, Caprio S. Obesity, Growth, Development, Metabolic Disorder, and Insulin Resistance in Pediatrics. 2024, vol1:608-vol1:616. DOI: 10.1201/9781003437734-70.ChaptersNonalcoholic fatty liver diseaseType 2 diabetesInsulin resistanceAdolescent obesityAssociated with precocious pubertyDevelopment of prediabetesCardiometabolic risk factorsPathogenesis of insulin resistanceFatty liver diseasePrecocious pubertyClinical peculiaritiesPediatric obesityLiver diseaseRisk factorsGlobal health challengeMetabolic disordersObesityFatty liverPathological complicationsPotential mechanismsInsulinHealth challengesChildrenComplicationsDyslipidemia
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 mechanismsMellitusGlucocorticoid signaling and the impact of high-fat diet on adipogenesis in vivo
Babel N, Feldman B. Glucocorticoid signaling and the impact of high-fat diet on adipogenesis in vivo. Steroids 2023, 201: 109336. PMID: 37944652, PMCID: PMC11005958, DOI: 10.1016/j.steroids.2023.109336.Peer-Reviewed Original ResearchObesity, Growth, Development, Metabolic Disorder, and Insulin Resistance in Pediatrics
Santoro N, Galderisi A, Caprio S. Obesity, Growth, Development, Metabolic Disorder, and Insulin Resistance in Pediatrics. 2023, 608-616. DOI: 10.1201/9781003437673-70.Peer-Reviewed Original ResearchNonalcoholic fatty liver diseaseType 2 diabetesInsulin resistanceAdolescent obesityCardiometabolic risk factorsMajor global health challengeFatty liver diseaseDevelopment of prediabetesGlobal health challengeClinical peculiaritiesFatty liverLiver diseasePediatric obesityRisk factorsPrecocious pubertyMetabolic disordersPathological complicationsObesityHealth challengesPsychosocial conditionsPotential mechanismsDiabetesEarly ageChildrenDyslipidemiaThe Effect of Aerobic Exercise on SREBP-1c Gene Expression in Skeletal Muscle in Obese Female Rats
Eftekharzadeh M, Atashak S, Azarbayjani M, Moradi L, Rahmati-Ahmadabad S. The Effect of Aerobic Exercise on SREBP-1c Gene Expression in Skeletal Muscle in Obese Female Rats. Thrita 2023, 12 DOI: 10.5812/thrita-138382.Peer-Reviewed Original ResearchEffects of aerobic exerciseAerobic exerciseHigh-fat dietSkeletal muscle metabolic disordersObese female ratsTreadmill 5 timesInteractive effects of aerobic exerciseMuscle metabolic disordersHigh-fatFemale ratsAerobic trainingSkeletal muscleQuadriceps muscleSREBP-1c geneSREBP-1c gene expressionNormal dietTraining sessionsMetabolic disordersExerciseSterol regulatory element-binding proteinFemale Wistar ratsWeight of ratsLipid metabolismQuadricepsSREBP-1cTime-restricted feeding combined with resistance exercise prevents obesity and improves lipid metabolism in the liver of mice fed a high-fat diet
Damasceno de Lima R, Fudoli Lins Vieira R, Rosetto Muñoz V, Chaix A, Azevedo Macedo A, Calheiros Antunes G, Felonato M, Rosseto Braga R, Castelo Branco Ramos Nakandakari S, Calais Gaspar R, Ramos da Silva A, Esper Cintra D, Pereira de Moura L, Mekary R, Rochete Ropelle E, Pauli J. Time-restricted feeding combined with resistance exercise prevents obesity and improves lipid metabolism in the liver of mice fed a high-fat diet. AJP Endocrinology And Metabolism 2023, 325: e513-e528. PMID: 37755454, DOI: 10.1152/ajpendo.00129.2023.Peer-Reviewed Original ResearchConceptsNonalcoholic fatty liver diseaseResistance exercise trainingTime-restricted feedingFatty liver diseaseHigh-fat dietLiver diseaseExercise trainingWeight gainGlycemic homeostasisMetabolic disordersEffects of TRFCommon liver diseaseDiet-induced obesityMajor risk factorEnergy expenditureFatty acid oxidation genesLiver of miceAccumulation of fatBody weight gainRespiratory exchange rateAccumulation of lipidsLower mRNA expressionRT groupPrevents obesityRisk factorsInactivation of Minar2 in mice hyperactivates mTOR signaling and results in obesity
Lotfollahzadeh S, Xia C, Amraei R, Hua N, Kandror K, Farmer S, Wei W, Costello C, Chitalia V, Rahimi N. Inactivation of Minar2 in mice hyperactivates mTOR signaling and results in obesity. Molecular Metabolism 2023, 73: 101744. PMID: 37245847, PMCID: PMC10267597, DOI: 10.1016/j.molmet.2023.101744.Peer-Reviewed Original ResearchConceptsMTOR activationHigh-fat dietObesity-associated diseasesGlucose toleranceKO miceChronic diseasesPathophysiological roleBody fatMetabolic disordersHypertrophic adipocytesKnockout miceObesityAdipose tissuePhysiological negative regulatorType 2HEK-293 cellsImpaired expressionComplex disorderCell culture studiesAdipocytesDiseaseMiceDisordersMTORUnknown role
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