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InsulinOralHypoglycemicYEInsulinOralHypoglycemicYEDiabetes Agroupofsyndromescharacterizedbyhyperglycemia,alteredmetabolismoflipids,carbohydratesandproteinsandincreasedriskofcomplicationsfromvasculardisease.Associatedwitharelativeorabsoluteinsufficiencyofinsulinsecretionwithvariousdegreesofinsulin.PreviousClassificationofDiabetesTypeI:insulin-dependentdiabetesmellitus(IDDM,ßcellsdysfunction)TypeII:Non-insulin-dependentdiabetesmellitusNIDDM,ßcellsnormalorhypofunction,Insulin Accountsformorethan95%pts。Clinical①fastinghyperglycemia(空腹高血糖②atheroscleroticandmicroangiopathicvasculardisease,complications(并发症)ofThechronichyperglycemiaofdiabetesisassociatedwithlong-termdamage,dysfunction,andfailureofvariousorgans,especiallytheeyes,kidneys,nerves,heartandbloodvessels.InJuly1997,TheAmericanDiabetesAssociationadoptedthefollowingguidelinesfortheclassificationofdiabetestypes,basedonType1-resultsfromanautoimmuneresponsetopancreaticß-cellcomponent(s)triggeredbyviralType2-hyperglycemiamaybedueIncreasedhepaticglucoseImpairedinsulinReceptorandpostreceptordefects)Now1.Type1diabetes-~10%ofallpatients-celldestructionleadingtoabsoluteinsulinImmunemediatedorIdiopathic(特发性2.Type2diabetes-~90%ofallMayrangefrompredominantlyinsulinresistantwithinsulindeficiencytoapredominantlysecretorydefectwith.Largergeneticcomponentthantype3.OtherspecificIncludesgeneticdefectsof-cellfunction,geneticdefectsofinsulinaction,exocrinepancreaticdisease,endocrinopathies,drug-orchemicalinducedforms,infections,andothergeneticdefectssometimesassociatedwithdiabetesmellitus.e.g.,MaturityOnsetDiabetesofYouth=Glucokinase-increasedthresholdforinsulinsecretion,causingmild,CausesofAbnormalß-cellsecretoryAbnormalinsulinpleteconversionofproinsulintoCirculatinginsulinElevatedlevelsofcounterregulatoryhormones, growthhormone,cortisol,glucagon,orAnti-insulinAnti-insulinreceptortissueInsulinreceptordefectsorPostreceptor21stCenturytype2diabetesinHowtodealwithComprehensivePhysicalDrugoralhypoglycemic(antihyperglycemic)agentswhichincreasethesensitivityoforganstoinsulin§1InsulinIns胰岛素secretedbyßcellsinthepancreaticislets,acidicprotein Thebirthofan InOctober,1920FrederickBanting,ayoungsurgeoninOntario,Canada,firstconceivedtheideathatledtothediscoveryofOneevening,afterdeliveringalectureonthepancreasmedicalstudents,hewasstruckbyanCouldtheinternalsecretionsofthepancreasbeisolatedfromtheexternalsecretionstokeepdogswithdiabetesalive?-tie-off(结扎)pancreaticductstocauseacinar(腺泡)tissuedegeneration,therebyremovingproteaseswhichweredestroyingtheanti-diabeticprincipleduringitsextraction(提取).BantingbeganhisresearchonMay19,1921,withMacleodasformalsupervisorandCharlesBestashisassistant.InAugustof1921afternumerousfailures,BantingandBestpreparedanewextractfromtheatrophiedpancreasofoneofthedogs.Theythenisolatedtwootherdogswithdiabetes,administeringtheextracttooneandleavingtheseconduntreated.Fourdayslater,theuntreateddogdiedofseverediabetes.Thedogthatreceivedtheextractlivedforthreemoreweeks,dyingonlywhentheextractwasusedup.FirstHumanOnJan.11,1922,14-year-oldLeonardThompsonwasthefirsthumanpatienttoreceiveinsulinmadebyBantingandTheinitialtestfailed,causingonlyslightreductionsinbloodglucoselevels.Asecondseriesof"purified"insulininjections,producedJ.B.Collip,achievedthedesiredLeonard'sbloodglucosedroppedtonormal,andhebegantogainweight.StructureofConsistsof2polypeptidechains(AandB)connectedbydisulfidebondsAnimal binantInsulinActionI.MajorregulatorofoverallbodyfuelIncreasedglycogensynthesis–forcesstorageofglucoseinliver(andmuscle)cellsintheformofglycogen;Decreasedgluconeogenesis–decreasesproductionofglucosefromnon-sugarsubstratesIncreasedfattyacidsynthesis–insulinforcesfatcellstotakeinbloodlipidswhichareconvertedtotriglycerides;Increasedesterificationoffattyacids–forcesadiposetissuetomakefats(i.e.,triglycerides)fromfattyacidesters;Decreasedlipolysis–forcesreductioninconversionoffatcelllipidstoresintobloodfattyacids;Decreasedproteolysis–decreasingthebreakdownofprotein.Increasedproteinsynthesis.Increasesaminoacidtransport.EffectsonK+MetabolicEffectsof

StimulatedbyIncreasedby

InhibitedbyinsulinIncreasedbyfastingand

Insulinbindstoansubunitoftheinsulinactivatingthetyrosine onsubunitsautophosphorylationleadstoactivationofcellulareffectorsandabiologicresponse.AkeyresponseisrecruitmentofglucosetransporterstothecellsurfaceinskeletalmuscleandadiposetissueNocompetitiveantagonistsorpartialagonistsofinsulinexistuntilnowOralinsulin-mimetichasbeenMechanismofInsulinRecruitmentofProtein:ProteinSignalTransductionNetworksActivationofPhosphorylationCascadesBiologicResponse

SkeletalAdipose

P PPPIRS-

NooralSubcutaneouslyinjection,ori.vt1/29—Metabolizedatliverandkidney.Orhydrolyzedbyinsulinase(whatanti-insulinasewilldo?)Clinical1.insulinType1Type2diabetescan’tcontrolbyotherDiabeteswithcomplicationketoacidosis )orhyperosmolarcoma(高 DiabeteswithIntracellularK+InsulininjectionShort-regularinsulin(正规胰岛素i.vavailablelisproinsulin(赖脯胰岛素Median-Lanteinsulin(低精蛋白锌胰岛素globinzincinsulin(珠蛋白锌混悬液Long-Protaminezincinsulin,(精蛋白锌胰岛素ponentinsulin(单组分:纯度高2.InsulinMarketat2006,lowF,9%,smokingcanincreaseFAdverse1allergic23 dosage>200U/ :relatedwithChronic :antibodytoinsulinreceptorsordecreasedantibodynumbers.4adipose§2OralHypoglycemicInsulin甲苯磺丁脲,D860);glibenclamide,glipizideAlpha-glucosidase(葡糖苷酶)inhibitors:Prandial(膳食glucose一、InsulinThiazolidinediones(噻唑烷酮类化合物)bindtoPPARγ(过氧化物酶增殖体受体γ)atypeofnuclearregulatoryproteinsinvolvedintranscriptionofgenesregulatingglucoseandfatmetabolism. ThesePPARsactonPeroxysomeProliferatorResponsiveElements(PPRE),influenceinsulinsensitivegenes,whichenhanceproductionofmRNAsofinsulindependentenzymes.Thefinalresultisbetteruseofglucosebythecells.Decreasethe intype2 rosiglitazone(罗格列酮 troglitazone(曲格列酮Pharmacological 1、improveinsulin ,reducetheblood 2、correctlipidmetabolism 3、preventinsulin 4、improvethefunctionofBcellsdecreasethe Clinical TypeIIdiabetesor Adverse Drowsy,headache,edema,muscular digestivesystem Hepatotoxicity,effecton Pharmacological1hypoglycemiafornormalandtype2diabeticpeople,facilitatesecretionofinsulinfrompancreaticislets,2antidiuresischlorpropamide氯磺丙脲),promotesecretionofADH3onblood:inhibitpla etadherenceincreasethesynthesisofprofibrinolysinMechanismofTheyareinsulinsecretagogues,triggeringinsulinreleasebydirectactionontheKATPchannelofthepancreaticbetacells.Byblockingthechannels,lessK+flowoutofcellsleadtomembranetheCa++channelopening,increasedintracellular++triggeringinsulinInhibitthesecretionofglucagon(胰高血糖素Upregulationofinsulinreceptors ClinicalDiabetes:typeIIdiabeteswithafewpancreaticfunctionorcan’tcontrolonDiabetesinspidus(尿崩症):AdverseGIoutofcondition,allergicLiverdamage&Blooddisorder,decreases et&Long-lasting , 地区食品药品监督管理局接到莎车县食品药品监督管理局报告。报告称接到莎车县卫生局报告一名叫叶丹的男子租借房屋,以“中国慢 康复 ”据查:该中国慢 康复 不存在的名义进讲课、诊疗 ,并对听课 免费检测血糖,暗地销售药品糖脂宁胶囊”:B0069,生产企业:广西平南制药厂,批号: DrugHighproteinbinding,interactionwithotherdrugs。IncreasedhypoglycemiceffectwithSomedrugcandecreasetheeffects:glucocorticoids,chlorpromazinemetformin(甲福明)、

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