简介：AbstractType 2 diabetes mellitus and metabolic disorders have become an epidemic globally. However, the pathogenesis remains largely unclear and the prevention and treatment are still limited. In addition to environmental factors during adulthood, early life is the critical developmental window with high tissue plasticity, which might be modified by external environmental cues. Substantial evidence has demonstrated the vital role of early-life nutrition in programming the metabolic disorders in later life. In this review, we aim to overview the concepts of fetal programming and investigate the effects of early-life nutrition on energy metabolism in later life and the potential epigenetic mechanism. The related studies published on PubMed database up to March 2020 were included. The results showed that both maternal overnutrition and undernutrition increased the riskes of metabolic disorders in offspring and epigenetic modifications, including DNA methylation, miRNAs, and histone modification, might be the vital mediators. The beneficial effects of early-life lifestyle modifications as well as dietary and nutritional interventions on these deleterious metabolic remolding were initially observed. Overall, characterizing the early-life malnutrition that reshapes metabolic disease trajectories may yield novel targets for early prevention and intervention and provide a new point of view to the energy metabolism.

简介：BACKGROUND:Duringthecellularagingprocess,thenumberofmitochondria,generationofadenosinetriphosphate(ATP),activityofrespiratorychainenzymecomplex1and4,andoxidationdecrease.OBJECTIVE:Toobservetheeffectsofaqueousandspirituousextract,aswellaspolysaccharidesfromFructusschizandrae(MagnoliaVine)onenergymetabolismandmitochondrialanti-oxidationincranialnervecellsofaD-gal-inducedagingmousemodel.DESIGN,TIMEANDSETTING:Arandomized,controlled,animalstudy.TheexperimentwasconductedattheDepartmentofBiochemistry,QiqiharMedicalCollegebetweenMarchandJuly2006.MATERIALS:Fiftyhealthy,Kunmingmiceofbothsexes,aged2-3monthsoldandweighing18-22g,wereusedforthepresentstudy.FructusschizandraewaspurchasedfromtheMedicalCollegeofJiamusiUniversity.Aqueousextracts,spirituousextracts,andpolysaccharidesfromFructusschizandraewereprepared.D-galactose(D-gal)isaproductoftheSecondReagentFactory,ShanghaiCity,China.Mn-superoxidedismutase(Mn-SOD)kit,malonaldehyde(MDA)kit,proteinquantificationkit,andinorganicphosphorustestingkitwerepurchasedfromJianChengBioeng.Co.,China.METHODS:Fiftymicewererandomlydividedintofivegroups,with10miceineachgroup:youngcontrol,agingmodel,aqueousFructusschizandraeextract,spirituousFructusschizandraeextract,andFructusschizandraepolysaccharides.Overacourseof30days,miceinagingmodel,aqueousFructusschizandraeextract,spirituousFructusschizandraeextract,andFructusschizandraepolysaccharidesgroupswereinjectedsubcutaneouslywithD-gal(100mg/kg)intothenapeoftheneckdaily,andadministeredintragastricallywithanequalvolumeofsterile,warmwater(agingmodel),aqueousFructusschizandraeextract(2g/kg),spirituousFructusschizandraeextract(2g/kg),orFructusschizandraepolysaccharides(0.2g/kg),respectively.Miceintheyoungcontrolgroupwereinjectedintothenapeoftheneckwithphysiologicalsaline

简介：Recentstudieshaverevealedthatthepropertyofdrugismainlyassociatedwiththebody'ssubstanceandenergyme-tabolism.ThepresentstudyaimedtoevaluatethedrugpropertyofPoria,calledFuling(FL)intraditionalChinesemedicine(TCM),intermsofitseffectsonthesubstanceandenergymetabolisminratmodelsofcold-deficiencyandheat-deficiencysyndromes,comparedwithAconitiLateralisRadixPraeparaia,calledFuzi(FZ)inTCM,withhotproperty,andAnemarrhenaeRhizoma,calledZhimu(ZM)inTCM,withcoldproperty,asreferencedrugs,respectively.Theappearancescore,toeandrectaltemperaturesoftheanimalstreatedwereassessedatdifferenttimepoints.Severalindicesinvivocorrelatedwithsubstanceandenergymetabolism(glucokinas,phosphoglyceratekinase,cytochromecreductase,cytochromecoxydase,andNa^+-K^+-ATPase),endocrinesystem(triiodothyronine,thyroxine,and17-hydroxycorticosteroid),nervoussystem(acetylcholinesterase),andcyclicnucleotidesystemweredetermined.Thechangesinappearancescoreandindicesinvivosuggestedthesuccessfulestablishmentofcold-deficiencyandheat-deficiencysyndromemodels.FZreversedthedecreasedlevelsofindices(substanceandenergymetabolismandendocrinesystem)andalleviatedthesyndromeofcold-deficiencymodel,andZMshowedobviouslytherapeuticeffectonheat-deficiencysyndrome(appearancescore,substanceandenergymetabolism,andendocrinesystem).FLcouldalleviatecold-deficiencysyndromeandraisethedecreasedlevelsofglucokinas,phosphoglyceratekinase,cytochromecreductaseandtriiodothyronineincold-deficiencymodel,buthadnosignificanteffectonheat-deficiencysyndrome.DrugpropertyofFLwasinferredastrendingto"flatandwarm",whichstillneedfurtherstudy.Itwasadvisabletoadoptbothcold-deficiencyandheat-deficiencymodelstostudythedrugswith"flat"property.

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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.

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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：Themediumaccesscontrol(MAC)protocolforindoorvisiblelightcommunication(VLC)withenergyharvestingisexploredinthispaper.Theunfairnessofthroughputexistsamongdevicesduetothesignificantdifferenceoftheirenergyharvestingrateswhichchangeswithdistance,acceptanceangleandtheobstructionprobability.Weproposeanenergyharvestingmodel,anewobstructionprobabilitymodelandanenergyadaptivecontentionalgorithmtoovercometheunfairnessproblem.Thisdevicecanadjustitscontentionwindowaccordingtotheenergyharvestingrate.Asaresult,thedevicewithlowerenergyharvestingratecangetshortercontentionwindowtoimproveitstransmissionopportunity.SimulationresultsshowthatourMACprotocolcanachieveahigherdegreeoffairness.