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简介：AbstractMelanoma originates from epidermal melanocytes and is the most malignant form of skin cancer, with an increasing incidence worldwide. In addition to the known pathological mutations in melanoma, the remodeling of epigenetic modification has recently been documented to orchestrate the malignant behaviors of tumor cells and anti-tumor immunity, emerging as an irreversible tumorigenic event that is more preventable and treatable with medications. As a hallmark characteristic of cancer, the disorder of cellular metabolism is also greatly implicated in tumor carcinogenesis and development. Accumulating evidence has revealed the close linkage between metabolism and epigenetics in multiple biological activities. In the pathogenesis of melanoma, the findings of other groups and our laboratory highlight the pivotal role of autophagy, mitochondrial function, and the oncometabolite acetyl-CoA, as well as their epigenetic modification. Targeted metabolism-associated epigenetic modulation might be a novel approach for melanoma therapy in the future.

简介：<正>Researchinpaediatricexercisemetabolismhasbeenconstrainedbybeingunabletointerrogatemuscleinvivo.Conventionally,researchhasbeenlimitedtotheestimationofmusclemetabolismfromobservationsofbloodandrespiratorygasesduringmaximalorsteadystateexerciseandtheanalysisofafewmusclebiopsiestakenatrestorpost-exercise.Thepurposeofthispaperistoreviewhowtheintroductionof31P-magneticresonancespectroscopyandbreath-by-breathoxygenuptakekineticsstudieshascontributedtocurrentunderstandingofexercisemetabolismduringgrowthandmaturation.Methodologicallyrobuststudiesusing31P-magneticresonancespectroscopyandoxygenuptakekineticswithchildrenaresparseandsomedataareinconflict.However,itcanbeconcludedthatchildrenrespondtoexercisewithenhancedoxygenutilizationwithinthemyocytecomparedwithadultsandthattheirresponsesareconsistentwithagreaterrecruitmentoftypeImusclefibres.Changesinmusclemetabolismareage,maturation-andsex-relatedanddependentontheintensityoftheexercisechallenge.Theintroductionofexperimentalmodelssuchas"primingexercise"and"work-to-work"transitionsprovideintriguingavenuesofresearchintothemechanismsunderpinningexercisemetabolismduringgrowthandmaturation.

简介：<正>1IntroductionHaloarchaearepresentsadistinctgroupofArchaeathattypicallyinhabitshypersalineenvironments,suchassaltlakesandseasalterns.Theyareeasytocultureandmanyhaloarchaeaaregeneticallytractable,hencetheyareexcellentmodelsystemsforresearchofarchaealgenetics,

简介：AbstractPsoriasis is considered a systemic disease associated with metabolic abnormalities, and it is important to understand the mechanisms by which metabolism affects pathophysiological processes both holistically and systematically. Metabolites are closely related to disease phenotypes, especially in systemic diseases under multifactorial modulation. The emergence of metabolomics has provided information regarding metabolite changes in lesions and circulation and deepened our understanding of the association between metabolic reprogramming and psoriasis. Metabolomics has great potential for the development of effective biomarkers for clinical diagnosis, therapeutic monitoring, prediction of the efficacy of psoriasis management, and further discovery of new metabolism-based therapeutic targets.

简介：Neurodegenerationischaracterizedbytheprogressiveandpermanentlossofneurons.Degenerationtypicallyresultsinadebilitatinglossoffunctioninanotherwisehealthyperson.Neurodegenerativediseaseshaveenormousdirecthealthcarecosts,withsomeestimatesfordiseases,suchasAlzheimer’sdiseaseexceeding$36,000

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简介：AbstractPancreatic ductal adenocarcinoma (PDAC) is an extremely malignant disease, which has an extremely low survival rate of <9% in the United States. As a new hallmark of cancer, metabolism reprogramming exerts crucial impacts on PDAC development and progression. Notably, arginine metabolism is altered in PDAC cells and participates in vital signaling pathways. In addition, arginine and its metabolites including polyamine, creatine, agmatine, and nitric oxide regulate the proliferation, growth, autophagy, apoptosis, and metastasis of cancer cells. Due to the loss of argininosuccinate synthetase 1 (ASS1) expression, the key enzyme in arginine biosynthesis, arginine deprivation is regarded as a potential strategy for PDAC therapy. However, drug resistance develops during arginine depletion treatment, along with the re-expression of ASS1, metabolic dysfunction, and the appearance of anti-drug antibody. Additionally, arginase 1 exerts crucial roles in myeloid-derived suppressor cells, indicating its potential targeting by cancer immunotherapy. In this review, we introduce arginine metabolism and its impacts on PDAC cells. Also, we discuss the role of arginine metabolism in arginine deprivation therapy and immunotherapy for cancer.

简介：Objective:PyruvatekinasesM(PKM),includingthePKM1andPKM2isoforms,arecriticalfactorsinglucosemetabolism.PKM2promotesaerobicglycolysis,aphenomenonknownas"theWarburgeffect".ThepurposeofthisstudywastoidentifytherolesofPKM2inregulatingcellularmetabolism.Methods:TheCRISPR/Cas9systemwasusedtogeneratethePKM-knockoutcellmodeltoevaluatetheroleofPKMincellularmetabolism.LactatelevelsweremeasuredbytheVitrosLACslidemethodonanautoanalyzerandglucoselevelsweremeasuredbytheautoanalyzerAU5800.Themetabolismof13C6-glucoseor13C5-glutaminewasevaluatedbyliquidchromatography/massspectrometryanalyses.TheeffectsofPKMontumorgrowthweredetectedinvivoinatumor-bearingmousemodel.Results:WefoundthatbothPKM1andPKM2enabledaerobicglycolysis,butPKM2convertedglucosetolactatemuchmoreefficientlythanPKM1.Asaresult,PKM2reducedglucoselevelsreservedforintracellularutilization,particularlyfortheproductionofcitrate,andthusincreasedtheα-ketoglutarate/citrateratiotopromotethegenerationofglutamine-derivedacetylcoenzymeAthroughthereductivepathway.Furthermore,reductiveglutaminemetabolismfacilitatedcellproliferationunderhypoxiaconditions,whichsupportsinvivotumorgrowth.Inaddition,PKM-deletioninducedareverseWarburgeffectintumorassociatedstromalcells.Conclusions:PKM2playsacriticalroleinpromotingreductiveglutaminemetabolismandmaintainingprotonhomeostasis.ThisstudyishelpfultoincreasetheunderstandingofthephysiologicalroleofPKM2incancercells.

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简介：我们为在人的线粒体与氨基酸新陈代谢联系的新陈代谢的小径的鉴定和重建使用了一条生物信息学途径。试验性、计算的方法决定的人的mitochondrial蛋白质从KEGG数据库在参考小径上被迭加识别mitochondrial小径。在为每条重建的小径的入口和出口点的酶被识别，并且mitochondrial溶质搬运人蛋白质是坚定的在哪儿适用。在mitochondrial小径的中间的酶基于从公共数据库，在当前的文学的证据，或我们的MITOPRED程序可得到的注解被识别，它预言蛋白质的mitochondrial本地化。通过从试验性、文献、计算的来源导出的数据的集成，我们重建了氨基酸在人的线粒体的新陈代谢的小径，它帮助能更好处于人的健康理解mitochondrial新陈代谢和它的角色。

简介：瞄准：调查在有低于正常的睾丸激素的老人的s铺平的饭后的triglycerides(TG)的水平(≤11.0nmol/L)与有正常的人相比，睾丸激素铺平(>11.0nmol/L)。方法：Thirthy--与弱智一起的七个人和有60-80年的正常睾丸激素的41个人经历了口头的胖负担，TG层次以后是测量禁食和2，4，6和8h。结果：有低于正常的睾丸激素的人有显著地更高的身体团索引(BMI)和腰圆周(P<0.001)比有正常的人睾丸激素。他们在曲线下面有显著地更高的区域(AUC，P=0.037)，在曲线下面的增长区域(AUCi，P=0.035)并且TG反应(TGR，P=0.014)为serum-TG和显著地更高的AUC(P=0.023)，AUCi(P=0.023)并且TGR(P=0.014)为与有正常的人相比的chylomicron-TG，睾丸激素铺平。为腰圆周调整在饭后的triglyceridemia擦掉在这些组之间的有效差量。结论：有低于正常的睾丸激素的人增加了显示饭后的TG富有的脂蛋白(TRL)的损害新陈代谢的饭后的TG层次，它可以增加不利类脂化合物侧面并且支持动脉粥样硬化的开发。

简介：AbstractIt shows that detrimental exposures and conditions in mothers can lead to the development of obesity and type 2 diabetes in offspring. This can lead to a vicious cycle of metabolic dysfunction, where rising rates of obesity, pre-diabetes, and diabetes in individuals of reproductive age, propagating risks to subsequent generations. It is well established that regular exercise has important health benefits for people with obesity and type 2 diabetes. Recently, increasing studies aim to examine the effects of maternal exercise on metabolic health in offspring. This review aims to demonstrate the evidence linking maternal exercise during critical periods of development and its implications for glucose metabolism in offspring, including intervention timing, sexual dimorphism, different exercise type, and intensity. Then we further examine the potential role of epigenetic modifications in this process.

简介：Litopenaeusvannamei,aeuryhalinespecies,canbeculturedatawiderangeofsalinities.Theemergenceoffreshwaterpond-cultureofL.vannameiisanimportantpreludetothecontinueddevelopmentofshrimpcultureinChina.Inthisstudy,wecomparedtherespiratorymetabolismofjuvenileL.vannameiculturedinfreshwaterandsaltwaterbymeasuringtheiroxygenconsumptionrate(OCR),ammonium-typenitrogenexcretionrate(AER)andpyruvatekinase(PK)andlactatedehydrogenase(LDH)activitiesatdifferentmoltingstagesinordertophysiecologicallycharacterizejuvenileL.vannameiunderfreshwaterconditions.TheresultsshowedthatOCRwassignificantlyhigherinsaltwaterthaninfreshwateratallstagesofmoltingcycle.However,variationofOCRamongmoltingstagesinsaltwaterwassimilarwiththatinfreshwater,andthehighestOCRwasobservedatpost-moltingstage.Atallstagesofmoltingcycle,AERwassignificantlyhigherinfreshwaterthaninsaltwater,andthehighestwasobservedatpost-moltingstage.TheactivityofPKwassignificantlyhigherinsaltwaterthaninfreshwater.Conversely,theactivityofLDHwashigherinfreshwaterthaninsaltwateringeneral.SignificantvariationofPKandLDHactivitiesinmoltingcyclewasobservedinsaltwaterandfreshwater.TheresultsindicatedthataerobicmetabolismofjuvenileL.vannameiwasmoreactiveinsaltwaterthaninfreshwater;whileitsproteinmetabolismwasmoreactiveinfreshwaterthaninsaltwater.

简介：ObjectivesTodetectwhetherpersistingortransientglucosemetabolismdisorderisresponsibleforadmissionhyperglycemiainpatientswithacutemyocardicinfarction(AMI).MethodsTwogroupsofpatientswereenrolled:AMIgroupandcontrolgroup.Fastingplasmaglucose,2hoursplasmaglucose,glycatedalbumin(GA)andglycatedhaemoglobin(HbA1c)weremeasuredatbaselineinbothgroupsand30daysafterAMIattackinAMIgroup.Results(1)Therewerenosignificantdifferencesinbaselinecharacteristicsbetweenbothgroups;(2)Comparedwiththecontrolgroup,thelevelsofGAandHbAlcinAMIgroupatbaselineweresignificantlyhigher.(3)At30dayfollow-upinAMIgroup,bothFBGand2hPGdecreasedtonormalvalues,HbAlcdidnotchange,butonlyGAkeptonincreasing.ConclusionsHyperglycemiaonadmissioninpatientswithAMIresultedfrombothpreexistingmetabolicdisorderandstressreactionaswell.GAistheonlyindicatorthatcouldrecalltheexaggerationofglucosemetabolicdisorderduringAMIattackat30dayfollow-up.

简介：ObjectivesToinvestigateserumconcentrationofprocollagentypeIcarboxyterminalpeptide(PIP),typeⅢaminopeptide(PⅢP)andtypeIcollagentelopeptide(ICTP)inessentialhypertension(EH).MethodsSerumlevelsofPIP,PⅢPandICTPin42EHpatientsand30healthycontrolweremeasuredbyradioimmunoassays.ResultsInEHpatients,serumconcentrationofPIP,PⅢPwassignificantlyhigherthanthatin30healthycontrol.AlthoughEHpatientsdidtendtoexhibitahigherserumICTPconcentrationthannormalcontrolsubjects,thedifferencewasnotstatisticallysignificant.EHpatientswithleftventricularhypertrophyexhibitedhighervaluesofPIP(P<0.05)andlowervaluesofICTP(P<0.05)thanEHpatientswithoutleftventricularhypertrophy.NosignificantdifferencewasnotedbetweentheserumPⅢPoftheEHpatientswithandwithoutleftventricularhypertrophy(P>0.05).ConclusionsTheresultssuggestthatPIPandPⅢParesensitiveserummarkersofmyocardialcollagensynthesis.Myocardialfibrosismaybeduetotheexcessivesynthesisandinsufficientdegradationofcollagen.PIP,PⅢPandICTPmaybeindirectmarkersofmyocardialfibrosis.

简介：AbstractTraumatic brain injury (TBI), a growing public health problem, is a leading cause of death and disability worldwide, although its prevention measures and clinical cares are substantially improved. Increasing evidence shows that TBI may increase the risk of mood disorders and neurodegenerative diseases, including Alzheimer's disease (AD). However, the complex relationship between TBI and AD remains elusive. Metabolic dysfunction has been the common pathology in both TBI and AD. On the one hand, TBI perturbs the glucose metabolism of the brain, and causes energy crisis and subsequent hyperglycolysis. On the other hand, glucose deprivation promotes amyloidogenesis via β-site APP cleaving enzyme-1 dependent mechanism, and triggers tau pathology and synaptic function. Recent findings suggest that TBI might facilitate Alzheimer's pathogenesis by altering metabolism, which provides clues to metabolic link between TBI and AD. In this review, we will explore how TBI-induced metabolic changes contribute to the development of AD.

简介：Anovertphenotypeofaquaporin-1knockout(AQP1ko)miceisgrowthretardation,suggestingpossibledefectsinbonedevelopmentandmetabolism.Inthepresentstudy,weanalyzedthebonemineraldensity(BMD),bonecalciumandphosphoruscontents,andbonemetabolisminanAQP1komousemodel.TheBMDoffemursinAQP1komicewassignificantlylowerthanthatoflitter-matchedwildtypemiceasmeasuredbydualenergyX-rayabsorptiometry.Consistently,thecontentsofbonetotalcalciumandphosphoruswerealsosignificantlylowerinAQP1komice.ThereducedBMDcausedbyAQP1deficiencymainlyaffectmalemice.Bonemetabolicactivity,asindicatedby99mTc-MDPabsorptionmeasurements,wasremarkablyreducedinAQP1komice.TheseresultsprovidethefirstevidencethatAQP1playanimportantroleinbonestructureandmetabolism.

简介：BACKGROUND:ResearchesindicatethatpatientswithWilsondisease(WD)haveabnormalskeletalmetabolism,whichisinducedbyvariousfactors.OBJECTIVE:ToprobeintothechangingcharacteristicsofabnormalskeletalmetabolisminWDpatientsandobservetheeffectofdecoppertherapy.DESIGN:Case-contrastandself-controlstudy.SETTING:DepartmentofNeurology,AffiliatedHospitalofNeurologicalInstitute,AnhuiCollegeofTraditionalChineseMedicine.PARTICIPANTS:Atotalof35patientswithWDincluding21malesand14femalesagedfrom10to42yearswiththemeanageof(20±8)yearswereselectedfromDepartmentofNeurology,AffiliatedHospitalofNeurologicalInstitute,AnhuiCollegeofTraditionalChineseMedicinefromSeptember2000toFebruary2001.Allthepatientswereincompliancewiththediagnosticcriteria:historyoffamilyheredity;conesymptomsinvitro,physicalsignorliversymptoms;positiveKayser-Fleischerring;serumcopperprotein＜200mg/LorAcopperoxidase＜0.2;urinecopper＞1.6μmol/24hours;livercopper＞250μg/g(dryweight).Thecontrolgroupwasselectedfrom25casesofhealthindividualsincluding13malesand12femalesagedfrom16to35yearswiththemeanageof(22±6)years.Allpatientswhoparticipatedinthestudywereinformedfirstandconsented.METHODS:Patientsintreatmentgroupweretreatedwithvenousinjectionof1.0gsodiumdimercaptosulfonate,onceadayfortotally6successivedays.Andthen,patientsrestedfor2days.Thisprocedurementionedabovewasregardedasacourse,andthetreatmentlastedfor4-8courses.Beforeandafterinjectionofsodiumdimercaptosulfonate,serumcalcitonin(CT),osteocalcin(BGP),parathyroidhormone(PTH)and1,25-(OH)2VitD3weremeasuredwithradio-immunitymethod:blood,urinecalcium,phosphorumandurinecreatinineweremeasuredwithbiochemicalanalyzer;urinedihydropyrimidinedehydrogenase(DPD)wasdetectedwithenzyme-immunitymethod;bonemineraldensity(BMD)wascheckedattheonethirdfromdistalendofulnaandradiuswithsingle