新型糖尿病治疗药物：糖尿病药物设计的希望

NovelTherapeuticAgentsforManagementofDiabetesMellitus:AHopeforDrugDesigningagainstDiabetesMellitus新型糖尿病治疗药物：糖尿病药物设计的希望Life2025-03-15文献发表信息发表类型：JournalArticle、Review期刊：Life发表日期：08-1-2024关键词：糖尿病、治疗学、新药、干细胞、免疫疗法和植物疗法作者：AhmedM.E.Elkhalifa、AhmedM.E.Elkhalifa、MehakNazar、SofiImtiyazAli、IbraqKhursheed、..、ShowkatUlNabi作者单位：1.DepartmentofPublicHealth,CollegeofHealthSciences,SaudiElectronicUniversity,Riyadh11673,SaudiArabia;a.alkhalifa@.sa2.DepartmentofHaematology,FacultyofMedicalLaboratorySciences,UniversityofElImamElMahdi,Kosti1158,Sudan;lhmelamin@3.PreclinicalResearchLaboratory,DepartmentofClinicalVeterinaryMedicine,Ethics&Jurisprudence,Sher-e-KashmirUniversityofAgriculturalSciencesandTechnology(SKUAST-Kashmir),Srinagar190006,India;mehaknazar2422@(M.N.);imtiyazali@skuastkashmir.ac.in(S.I.A.);syedtaifa786@(S.T.);mahimuzaffar111@(M.A.M.);iqrahussainshah@(I.H.S.);drmasoodmalik16@(M.M.);zahidramzan367@(Z.R.);shubeenaahad786@(S.A.);nusratbashir510@(N.B.)文献重点信息摘取糖尿病（DM）的特征是胰岛素分泌和外周阻力绝对下降，是最常见的代谢和内分泌疾病。糖尿病的发病机制还包括脂肪细胞胰岛素抵抗、胰高血糖素分泌增加、肾小球葡萄糖吸收增加和神经递质功能障碍。尽管有各种各样的治疗方法可用于血糖控制，但由于确定了糖尿病的各种致病决定因素，糖尿病的管理仍然具有挑战性和复杂性。目前针对糖尿病的治疗干预主要集中在血糖控制上，而没有考虑最终导致治疗失败和糖尿病进展的其他病理决定因素。目前的综述文章讨论了新的治疗方案，这些方案特别有希望支持其安全性，并讨论了使用这些药物产生的副作用，以便将这些新的候选药物有效地制成治疗糖尿病的潜在药物。主要背景关于胰岛素缺乏症，糖尿病已被分为1型糖尿病（T1DM），也称为胰岛素依赖型糖尿病/青少年发病型糖尿病，与胰腺β细胞的自身免疫性破坏有关，存在于5-10%的糖尿病患者中。最近，有报道称，TIDM死亡率和发病率的增加与低社会人口状况有关。2型糖尿病（T2DM）也被认为是胰岛素非依赖型糖尿病（NIDDM）/成熟型糖尿病是各发达国家死亡的第四大原因，与冠心病和中风等心脏病的可能性并列。妊娠期糖尿病（GDM）是在怀孕期间观察到的，由于葡萄糖不耐受而发生，随后导致严重程度不同的高血糖症。该疾病的特征包括自身免疫反应，即身体的免疫系统攻击并破坏胰腺中产生胰岛素的β细胞，成人发病，逐渐发病和胰岛素依赖。对于无法通过改变生活方式和口服降糖药物达到血糖目标的患者，胰岛素治疗已被提倡。主要背景—相关文献参考(PMID:26868137)标题：糖尿病作为使用肾素-血管紧张素系统阻滞剂的重要适应症：随机试验的系统回顾和荟萃分析。期刊：BMJ(Clinicalresearched.)(影响因子：105.7)发表日期：2016-02-11第一单位：NewYorkUniversitySchoolofMedicine,NewYork,NY,USAsripalbangalore@.KeyMessages：PubMed、Embase和Cochrane中央对照试验数据库，用于糖尿病患者中RAS阻断剂与其他抗高血压药物的随机试验。与其他抗高血压药物相比，RAS阻断剂与死亡风险相似（相对风险0.99，95%可信区间0.93-1.05），心血管死亡（1.02，0.83-1.24），心肌梗死（0.87，0.64-1.18），心绞痛（0.80，0.58-1.11），中风（1.04，0.92-1.17），心力衰竭（0.90，0.76至1.07），以及血运重建（0.97，0.77至1.22）。在糖尿病患者中，RAS阻滞剂在降低心血管和肾脏硬终点风险方面并不优于其他抗高血压药物，如噻嗪类、钙通道阻滞剂和β受体阻滞剂。主要背景—相关文献参考(PMID:23376836)标题：橙皮素对糖尿病大鼠视网膜氧化应激、神经炎症和细胞凋亡的保护作用。期刊：Microvascularresearch(影响因子：3.1)发表日期：2013-05-01第一单位：DepartmentofPharmacology,DelhiInstituteofPharmaceuticalSciences&Research,UniversityofDelhi,NewDelhi,India.binitkumar35@KeyMessages：用热休克蛋白（100mg/kg体重）处理STZ诱导的糖尿病大鼠24周，观察抗氧化（超氧化物歧化酶、SOD、过氧化氢酶、CAT和谷胱甘肽、GSH）酶、炎性细胞因子（TNF-α、IL-1β）、caspase-3、胶质纤维酸性蛋白（GFAP）和水通道蛋白4（AQP4）的表达。而Hsp治疗的视网膜细胞因子水平明显低于糖尿病视网膜。2.目前的抗糖尿病治疗方案Table1：用于治疗糖尿病的商业药物及其相关作用机制，具有优缺点。治疗糖尿病的可用药物治疗包括胰岛素和各种口服降糖药，如磺脲类、二甲双胍、α-葡萄糖苷酶抑制剂（阿卡波糖和曲格列酮）和吡格列酮/罗格列酮[31]（表1和表2）。表1、表3和表4给出了改善和治疗糖尿病最常用的常规治疗剂的综合表，简要介绍了它们的优缺点。AlphaGlucosidaseInhibitorsDrugsTheseAreBuddingTherapeuticsAimedatBlockingα-Glucosidase,Henceforth,PostponingBreakdownofCarbohydratesWhichConsequentlyDiminishesItsIntestinalAssimilation[5]CommercialNameTheseAreBuddingTherapeuticsAimedatBlockingα-Glucosidase,Henceforth,PostponingBreakdownofCarbohydratesWhichConsequentlyDiminishesItsIntestinalAssimilation[5]MechanismofActionTheseAreBuddingTherapeuticsAimedatBlockingα-Glucosidase,Henceforth,PostponingBreakdownofCarbohydratesWhichConsequentlyDiminishesItsIntestinalAssimilation[5]AdvantagesTheseAreBuddingTherapeuticsAimedatBlockingα-Glucosidase,Henceforth,PostponingBreakdownofCarbohydratesWhichConsequentlyDiminishesItsIntestinalAssimilation[5]SideEffectsTheseAreBuddingTherapeuticsAimedatBlockingα-Glucosidase,Henceforth,PostponingBreakdownofCarbohydratesWhichConsequentlyDiminishesItsIntestinalAssimilation[5]References(a)AcarbosePrecoseThereisamendableblockageofglucosidasesesp.glucoamylase,sucrose,maltose,andα-amylaseofbrushborderepitheliumDecreasedpostprandialhyperglycemiainT2DMBorborygmic,abdominalfullness,diarrhea,intestinalflatulence[32](b)MigtitolGlycetWorksbyreducingthedisintegrationandassimilationofsugarinsmallintestineConsiderablehypoglycemiabyachievementofnormoglycemiainpatientsviaenhancementofglucosetoleranceLesserGITafter-effects[5,27,33](c)VogliboseNewlyaddedsignificantsucroseblockerSlowsdowntheglucoseassimilation,accordinglydecreasingthepossibilityofmacrovascularcomplications[5](d)InsulinsensitizersAidtheactivityofinsulininliver,adiposetissue,andmusclesinadditiontodecreasingtheperipheralinsulinresistanceinskeletalmusclesandadipocytesHypoglycemia,weightgain,diarrhea,andgreaterchanceofcardiovasculardiseases[34]2.目前的抗糖尿病治疗方案Table2：磺酰脲类药物用于治疗糖尿病及其相关作用机制，具有优缺点。治疗糖尿病的可用药物治疗包括胰岛素和各种口服降糖药，如磺脲类、二甲双胍、α-葡萄糖苷酶抑制剂（阿卡波糖和曲格列酮）和吡格列酮/罗格列酮[31]（表1和表2）。SulfonylureasDrugsSulfonylureasAreaClassofOralAntidiabeticDrugsCommonlyUsedintheTreatmentofType2Diabetes.TheyWorkbyStimulatingInsulinReleasefromtheBetaCellsofthePancreasCommercialNameSulfonylureasAreaClassofOralAntidiabeticDrugsCommonlyUsedintheTreatmentofType2Diabetes.TheyWorkbyStimulatingInsulinReleasefromtheBetaCellsofthePancreasMechanismofActionSulfonylureasAreaClassofOralAntidiabeticDrugsCommonlyUsedintheTreatmentofType2Diabetes.TheyWorkbyStimulatingInsulinReleasefromtheBetaCellsofthePancreasAdvantagesSulfonylureasAreaClassofOralAntidiabeticDrugsCommonlyUsedintheTreatmentofType2Diabetes.TheyWorkbyStimulatingInsulinReleasefromtheBetaCellsofthePancreasSideEffectsSulfonylureasAreaClassofOralAntidiabeticDrugsCommonlyUsedintheTreatmentofType2Diabetes.TheyWorkbyStimulatingInsulinReleasefromtheBetaCellsofthePancreasReferencesFirst-generationsulfonylureas(a)Chlorpropamide(b)Tolazamide(c)Tolbutamide(d)Acetohexamide(a)Diabinese(b)Tolinase(c)Orinase(d)DyemelorThesecausestimulationofthesecretionofinsulinfrompancreasConsiderablehypoglycemiaisachievedGITinterferencesandhemolyticanemia[22]2.Second-generationsulfonylureas(a)Glyburide(b)Glimepiride(c)Glipizide(a)Glynase(b)Gleam(c)GlucotrolAllofthesepromotethesecretionofinsulinfromβcellsofpancreasConsiderablehypoglycemiaisachievedGITinterferencesandhemolyticanemia[5,21,35]2.目前的抗糖尿病治疗方案Table3：双胍类药物用于治疗糖尿病及其相关作用机制，具有优缺点。表1、表3和表4给出了改善和治疗糖尿病最常用的常规治疗剂的综合表，简要介绍了它们的优缺点。BiguanidesDrugsTheyPrimarilyWorkbyReducingHepaticGlucoseProductionandImprovingPeripheralInsulinSensitivityMechanismofActionTheyPrimarilyWorkbyReducingHepaticGlucoseProductionandImprovingPeripheralInsulinSensitivityAdvantagesTheyPrimarilyWorkbyReducingHepaticGlucoseProductionandImprovingPeripheralInsulinSensitivitySideEffectsTheyPrimarilyWorkbyReducingHepaticGlucoseProductionandImprovingPeripheralInsulinSensitivityReferencesMetformin(extractedfromplantGalegaofficinalis)WorksbyimprovingtheserumglucoselevelsviahinderingtheliverglucoseproductionalongwithboostingtheuptakeofglucosebymusclefibersDecliningtriglyceridesandlow-densitylipidsandhaslesserfrequencyofhypoglycemiaLacticacidosis,vitB12deficiency,congestiveheartfailure[9]2.目前的抗糖尿病治疗方案Table4：噻唑烷二酮类药物（TZD）用于治疗糖尿病及其相关作用机制的优缺点。表1、表3和表4给出了改善和治疗糖尿病最常用的常规治疗剂的综合表，简要介绍了它们的优缺点。Thiazolidinediones(TZD)DrugsTheseDrugsWorkbyTargetingthePeroxisomeProliferator-ActivatedReceptorGamma(PPAR-γ),aNuclearReceptorInvolvedinGlucoseandLipidMetabolismCommercialNameTheseDrugsWorkbyTargetingthePeroxisomeProliferator-ActivatedReceptorGamma(PPAR-γ),aNuclearReceptorInvolvedinGlucoseandLipidMetabolismMechanismofActionTheseDrugsWorkbyTargetingthePeroxisomeProliferator-ActivatedReceptorGamma(PPAR-γ),aNuclearReceptorInvolvedinGlucoseandLipidMetabolismAdvantagesTheseDrugsWorkbyTargetingthePeroxisomeProliferator-ActivatedReceptorGamma(PPAR-γ),aNuclearReceptorInvolvedinGlucoseandLipidMetabolismSideEffectsTheseDrugsWorkbyTargetingthePeroxisomeProliferator-ActivatedReceptorGamma(PPAR-γ),aNuclearReceptorInvolvedinGlucoseandLipidMetabolismReferencesTroglitazoneRosiglitazonePioglitazone(a)Rezulin(b)Avandia(c)ActosEnhancesinsulinsensitivityofalltargettissuesandactsasligandsforPPAR(peroxisomesproliferator-activatedgamma)complexlocatedinsidethenucleusEffectonplasmalow-densitylipids/cholesterol(a)ClassIII–IVheartfailure.(b)Fluidretention,peripheraledema(c)CHF(congestiveheartfailure)[5,38,39]2.目前的抗糖尿病治疗方案Table5：用于治疗糖尿病的新型肽类似物类药物及其相关作用机制，具有优缺点。本综述的结果将推动确定最新的糖尿病治疗方案，并阐明其在细胞水平和亚细胞水平上的作用机制（表5）。在本手稿的后续部分，我们讨论了未来可用于有效管理糖尿病的新型糖尿病治疗剂，其中一些治疗剂处于临床试验的第3阶段，一些处于临床前开发阶段（表5和表6）。PeptideAnaloguesDrugsTheseAnaloguesAreSyntheticCompoundsDesignedtoMimictheActionsofEndogenousPeptidesInvolvedinGlucoseHomeostasisMechanismofActionTheseAnaloguesAreSyntheticCompoundsDesignedtoMimictheActionsofEndogenousPeptidesInvolvedinGlucoseHomeostasisAdvantagesTheseAnaloguesAreSyntheticCompoundsDesignedtoMimictheActionsofEndogenousPeptidesInvolvedinGlucoseHomeostasisSideEffectsTheseAnaloguesAreSyntheticCompoundsDesignedtoMimictheActionsofEndogenousPeptidesInvolvedinGlucoseHomeostasisReferencesIncretinmimeticsLiberatedinripostetotheingestionoffood,elicitingtheglucose-inducedinsulinresponseAppetencedecreasingpositiveimpactoftheseagentsoncardiovascular,inflammation,andthecentralnervoussystemDoesnothindertheglucagonemission[43,44]Glucagon-likepeptideanalogsandagonists(GLP-1)Retardingthegastricclearing,boostingtheinsulinsecretionalongsidehamperingtheglucagonsecretionfrompancreasPreventsgastricacidsecretioninadditiontopromotinginsulinsecretionNotreported[35,45,46]Glucose-dependentinsulinotropicpolypeptideanalogs(GIP)TheseanalogsaresyntheticcompoundsdesignedtomimictheactionsofendogenouspeptidesinvolvedinglucosehomeostasisReducingthepostprandialglucoselevelsandglycosylatedhemoglobinLesserdangerofhypoglycemiawiththeuseofthisagent[20,47]DPP-4inhibitorsGIPproducedoutofthekcellsoftheuppersmallintestineworksbyaffectingthemetabolismoflipidsFastingplasmaglucoselevelsreducedalongwiththechangesinglycosylatedhemoglobinEffectslikevomitingandanorexia[8,12]LiraglutideActionviaenzymaticincretindisintegrationAgonistforreceptor(GLP-1)Appetencedecreasingpositiveimpactoftheseagentsoncardiovascular,inflammation,andthecentralnervoussystemComparedtotheshort-actingforms,long-actingoneshavelesschanceofcausinghypoglycemia[9,48,49,50]3.新型治疗药物Table6：用于治疗糖尿病的新型抗糖尿病药物及其相关作用机制，具有优缺点。在本手稿的后续部分，我们讨论了未来可用于有效管理糖尿病的新型糖尿病治疗剂，其中一些治疗剂处于临床试验的第3阶段，一些处于临床前开发阶段（表5和表6）。NovelAnti-DiabeticAgentsDrugsTheLatestDevelopmentsinPharmacotherapy,FocusingonInnovativeApproachesThatAddresstheComplexChallengesofDiabetesMechanismofActionTheLatestDevelopmentsinPharmacotherapy,FocusingonInnovativeApproachesThatAddresstheComplexChallengesofDiabetesAdvantagesTheLatestDevelopmentsinPharmacotherapy,FocusingonInnovativeApproachesThatAddresstheComplexChallengesofDiabetesSideEffectsTheLatestDevelopmentsinPharmacotherapy,FocusingonInnovativeApproachesThatAddresstheComplexChallengesofDiabetesReferencesAmylinanalogs(isletamyloidpolypeptideSignificantdeclineinthelevelsofglucoseinT1DMandT2DMDecreasesthebloodglucoselevelbyreducingtheglucagonsecretionUsedassolotherapyorsometimesincombinationwithorallyactiveanti-diabeticagents.[23,52,53,54]2.PramlintideSecretedandstoredincombinationwithinsulinandhinderingtheglucagonsecretioninadditiontoslowingdowntheunloadingofgastriccontentsIfthereissomebetacellfunctionremaining,thenatthattime,replacementcurativeaidedwithbasalinsulincanprovetobeusefulIncreasedarterialpressure,inducingkidneydysfunction,onsetofhypertension,boostingtheoccurrenceofdiabetesandhypothyroidism[23,52,53,54]3.Nitrate/NitriteMoleculesproducedfromL-arginineviatheenzymesnitricoxidesynthase(NOS)namelyinducible,neuronal,endothelial,andmitochondrialhavebeenobservedtoabatethelevelsoftriglyceridesinserumRegulationofTGlevelsinbloodPromotionoffatdepositioninliver[23,52,53,54]4.Antioxidanttherapy:vitaminE,vitaminC,andβcaroteneFastingplasmainsulinandHbA1clevelsaredeclinedbyadministrationofvitaminC.Moreover,thereisseentoberefinementofinsulinaction.Likewise,withtheadministrationofβcarotene,reductionofoxidativelow-densitylipidshasbeennotedNeweffectivetherapyforthecureofT2DMpatientsisantioxidanttherapy,whichmightreflectasignificantroleindiminishingthechancesofdiabetichyperglycemiaandthereafteritsassociateddrawbacks[23,52,53,54]5.FBPase(fructose1,6-bisphosphatase)inhibitorsModeofactionviainhibitingtheFBPaseenzyme(rate-limitingenzymeingluconeogenesispathway)Liverhyperplasia,liverhypertrophy,andlivercarcinogenesis[23,52,53,54]6.BromocriptineRecently,Swift-liberatedbromocriptineevolvedinfavorofT2DMameliorationbutthemodeofactionisnotclearyetTheliteraturehasprovedthatafter24weeksoftherapy,theaverageglycatedhemoglobinlevelsdeclinedby0.0%to0.2%[23,52,53,54]7.Imeglimin(yettopasstheclinicaltrial)Quiteeffectiveinthesensethatitstimulatesglucoseuptakeinmuscles,livergluconeogenesisisdepressedalongwithboostinthesugar-dependentinsulinreleaseHamperingoxidativephosphorylation[23,52,53,54]8.Peroxisomeproliferator-activatedreceptors(PPARs)Mostlyparticipatingincontrollingtheenergyhomeostasissupplementarytoreductionoftriglycerides[23,52,53,54]3.6.民族医学Table7：用于治疗糖尿病的植物药物制剂，植物部分应具有高水平的药理活性成分——为其治疗作用确定的活性成分，以及可能的作用机制。(1)不同植物化学物质及其作用方式的综合表如（表7）所示，它们被加工成潜在的药物（图3）。PhytomedicinewithFamilyPortionActiveChemicalConstituentsMechanismofActionReferencesAlliumcepa(Onion)AlliaceaeCormS-methylcysteinesulphoxideandallylpropyldisulfideArousetheactionofenzymeshexokinaseandreductaseinadditiontotheproductionofinsulin[66]CaricapapayaCaricaceaeSeedandextractofleaves------Alleviatewoundsinalloxan-induceddiabeticratsinadditiontoreducingtheserumglucoselevel[37]Catharantusroseus(Vincaroses)ApocynaceaeLeavesandtwigs-------Boostingthebiosynthesisofinsulinfromthepancreaticislets[91]AcaciaArabicaFabaceaeBarkandseedPolyphenolsandtanninsCommencementofinsulinsecretionfrompancreaticβcells[92]Alliumsativum(Garlic)AlliaceaeCormAllicinandallylpropyldisulfideModifiestheactionofenzymesglucose-6-phosphate,HMGCoAreductase,andhexokinase,inadditiontomanagingglucoselevelsinserumandtissues[51]Aloebarbadensis(Aloevera/Ghikanwar)LiliaceaeLeafBarbaloinandalloinRevitalizingtheprocessofhepatogluconeogenesis/glycogenolysisalongsidetheliberationofinsulinfromthepancreas.Inaddition,theglutathionelevelsindiabeticratswereelevatedbyafactorof4[4,63]Betavulgaris(Beetroot)RootBetacyaninsandphenolicsNon-enzymaticglycosylationofserumglucoseandskinproteinsdeclined[92]Azadirachtaindica(Neem)MeliaceaeSeedandleafNimbinandazadirachtinβcellsofthepancreasarerevived/revitalizedAlso,ithasbeennotedtoamendbloodcirculationviadilatingbloodvessels(Mishraetal.,2011)[93,94]Brassicanigra(Mustard)BrassicaceaeWholeplantSinignin,isorhamnetin,diglucoside,andisothiocynateTheconductofglycogensynthetaseisboostedunliketheactionofglycogenphosphorylaseandgluconeogenicenzymes,whichisreducedtherebydepressingglycogenolysisandgluconeogenesis[51]3.6.民族医学Table7：用于治疗糖尿病的植物药物制剂，植物部分应具有高水平的药理活性成分——为其治疗作用确定的活性成分，以及可能的作用机制。(2)不同植物化学物质及其作用方式的综合表如（表7）所示，它们被加工成潜在的药物（图3）。PhytomedicinewithFamilyPortionActiveChemicalConstituentsMechanismofActionReferencesCassiaauriculata(Senna)LeguminaceaeFlowerSennosideAandSennosedeBTheactivityofhepatichexokinaseandphosphofructokinaseenzymesisamplifiedwhiletheactivityofglucose-6-phosphateandfructose-1,6-biphosphataseenzymesissuppressed.Further,thereisanincreaseintheno.ofisletsandbetacellsinpancreas[51]AndrographisPaniculata(Kalmegh)AcanthaceaeWholeplantAndrographolide,kalmeghin,andditerpenoidlactoneGlucoseassimilationfromtheintestinalwalliscountered[51,62]Gymnemasylvestre(Gudmar)AsclepiadaceaeLeafGymnemasaponinsandgymnemicacidBoostingthenumberofβcellsalongwithinsulinsecretion[63]Ficusbenglenesis(Banyan)MoraceaeBarkandleafTannin,taraxasterol,quercetin-3-galactoside,andrutinBloodinsulinlevelsintype2diabetesmellitusweretriggeredviatheactionofhypoglycemiccomponentsseparated[63]Capsicumfrutescens(Mirch)SolanaceaeEntireplantorFruitCapsaicin,proteinThereisthedevaluationofinsulinbindingoninsulinreceptorsalongwithboostinginsulinvoiding[51]Coriandrumsativum(Corianderfruits)UmbelliferaeSeedBloodglucoseleveldeclinedincludingtheactivityofbetacellsescalatedthereafteraugmentinginsulinrelease[62]Cuminumcyminum(Jira)UmbelliferaceaeSeedGeraniol,coriandrol,pinene,coriendrlyacetateDepletioninglycosylatedhemoglobin,bloodureanitrogen,andbloodglucose,andatthesametimeseruminsulincontentisenhanced[62]Eucalyptusglobulas(Nilgiri,Dinkumoil)LeafHydrocumin,phellandrene,andcuminaldehydeElevationofperipheralglucoseuptake[61,92,95]CurcumalongaLe.(Turmeric)ZingiberaceaeTuberCitronella,camphene,pinene,cineoleMentionedmedicineshowedpromisingoutcomesinthemanagementofdiabetes[13,62]3.6.民族医学Table7：用于治疗糖尿病的植物药物制剂，植物部分应具有高水平的药理活性成分——为其治疗作用确定的活性成分，以及可能的作用机制。(3)不同植物化学物质及其作用方式的综合表如（表7）所示，它们被加工成潜在的药物（图3）。PhytomedicinewithFamilyPortionActiveChemicalConstituentsMechanismofActionReferencesEugeniajambolana(jamun)MyrtaceaeDriedseedandpulpEssentialoil,dimethoxycurcumin,curcumin,andBtermennoneIntensifyingtheemissionofinsulininadditiontohindranceoftheliverandkidneyenzymeinsulinase[96]TrigonellafoenumGraecum(Methi)LeguminosaeSeedOleanolicacid,ellagicacid,alphaglucosidase,Malvidin3-laminaribiosideaandferulicacidValuabledischargeofinsulinalongsidetheinducementofinsulincoalescence[51,97]TinosporacrispaMenispermaceaeStemNicotinicacid,coumarin,saponin-peptideesters,trigonelline,andflavonoidsStimulationofinsulinsecretiononaccountofitsanti-diabeticeffectandfurther,thereistheregulationofcalciumconcentrationofbetacells[51,62]OcimumsanctumL.(Tulsi)LamiaceaeLeafFraxinuscoumarinalkaloids,ascoacid,eugenol,andglucosideSerumglucoselevelisdiminished[62]Lawsoniainermis(Henna)LythraceaeSeedandflowerXanthonesandtannin,alkaloidsandfattyoilConcentrationofcholesterol,glucose,andtriglyceridesisdepressed[98]Momordicacharantia(Karela)CucurbitaceaeLeafCharantin,momordicI,momordicII,andcucurbitacinBTheremayberejuvenationofmoderatelydamagedcellsalongwithimprovementofbetacellproductioninthepancreas.Inaddition,saidproductcontainslectin,whichmimicstheactionofinsulin[92]MangiferaindicaAnacardiaceaeLeafMangiferinIntestinalabsorptionofglucoseisdecreased[42]Musasapientum(Banana)MusaceaeFlowerGlycoside,flavonoids,andsteroidWorksbysimulatinginsulin-likeaction[99]TinosporaCardifolia(Guduchi)MenispermaceaeRoot,stem,andleavesDiterpenoidlactones,alkaloid,glycosides,andsteroidsAppreciabledepressionofbloodsugar[100]3.6.民族医学Table7：用于治疗糖尿病的植物药物制剂，植物部分应具有高水平的药理活性成分——为其治疗作用确定的活性成分，以及可能的作用机制。(4)不同