AbMole小講堂丨Insulin：調(diào)控代謝的核心信號(hào)分子與其科研應(yīng)用Insulin（Human，AbMole，M9194）是一種由胰島β細(xì)胞合成和分泌的蛋白質(zhì)類激素，在生命體的代謝調(diào)控網(wǎng)絡(luò)中扮演著核心角色。Insulin可與靶細(xì)胞表面的Insulin受體（一種具有內(nèi)在酪氨酸激酶活性的跨膜蛋白）結(jié)合。當(dāng)Insulin與其受體結(jié)合后，會(huì)誘發(fā)受體構(gòu)象的變化，并引發(fā)受體β亞基的自身磷酸化，隨后激活下游的信號(hào)轉(zhuǎn)導(dǎo)級(jí)聯(lián)反應(yīng)，從而啟動(dòng)兩條關(guān)鍵的信號(hào)通路：PI3K/Akt通路和Ras/MAPK通路。其中，PI3K/Akt通路是Insulin產(chǎn)生代謝效應(yīng)的核心通路，它能夠促進(jìn)葡萄糖轉(zhuǎn)運(yùn)蛋白GLUT4向細(xì)胞膜的轉(zhuǎn)位，極大地加速細(xì)胞對(duì)葡萄糖的攝取與利用；同時(shí)，該通路通過調(diào)節(jié)一系列關(guān)鍵的酶和轉(zhuǎn)錄因子，促進(jìn)糖原、脂質(zhì)與蛋白質(zhì)的合成代謝，并抑制糖異生和脂肪分解等代謝過程。而Ras/MAPK通路則更多地與Insulin的促細(xì)胞生長、增殖與分化效應(yīng)相關(guān)ADDINEN.CITE<EndNote><Cite><Author>Petersen</Author><Year>2018</Year><RecNum>1344</RecNum><DisplayText><styleface="superscript">[1]</style></DisplayText><record><rec-number>1344</rec-number><foreign-keys><keyapp="EN"db-id="f2td9w00a22awteprfrp9vaup9d9zwa9tdfr"timestamp="1762240407">1344</key></foreign-keys><ref-typename="JournalArticle">17</ref-type><contributors><authors><author>Petersen,MaxC.</author><author>Shulman,GeraldI.</author></authors></contributors><titles><title>MechanismsofInsulinActionandInsulinResistance</title></titles><pages>2133-2223</pages><volume>98</volume><number>4</number><dates><year>2018</year></dates><accession-num>30067154</accession-num><urls><related-urls><url>/doi/abs/10.1152/physrev.00063.2017</url></related-urls></urls><electronic-resource-num>10.1152/physrev.00063.2017</electronic-resource-num></record></Cite></EndNote>[1]。Insulin（Cattle，AbMole，M9164）主要作為一種重要的生物活性分子在科研領(lǐng)域中被廣泛應(yīng)用。例如Insulin可用于構(gòu)建胰島素抵抗的細(xì)胞和動(dòng)物模型。有研究將脂肪細(xì)胞長期暴露于濃度為150nM的Insulin中，實(shí)現(xiàn)了體外胰島素抵抗模型的構(gòu)建ADDINEN.CITEADDINEN.CITE.DATA[2]。Insulin也可用于某些細(xì)胞的定向分化誘導(dǎo)，例如10μg/ml的Insulin、1μMDexamethasone、0.5mMIBMX（PDE抑制劑）和5μMRosiglitazone組成的分化培養(yǎng)基可以誘導(dǎo)前體脂肪細(xì)胞分化為成熟的脂肪細(xì)胞，這為研究脂肪細(xì)胞發(fā)育和代謝調(diào)控提供了重要的實(shí)驗(yàn)?zāi)Ｐ虯DDINEN.CITE<EndNote><Cite><Author>Qin</Author><Year>2015</Year><RecNum>1</RecNum><DisplayText><styleface="superscript">[3]</style></DisplayText><record><rec-number>1</rec-number><foreign-keys><keyapp="EN"db-id="xpw9pe9wgv020jer9t4pfw0cz5rvas9at5d9"timestamp="1762417376">1</key></foreign-keys><ref-typename="JournalArticle">17</ref-type><contributors><authors><author>Qin,Ji-Huan</author><author>Ma,Jun-Zeng</author><author>Yang,Xing-Wei</author><author>Hu,Ying-Jie</author><author>Zhou,Juan</author><author>Fu,Lin-Chun</author><author>Tian,Ru-Hua</author><author>Liu,Shan</author><author>Xu,Gang</author><author>Shen,Xiao-Ling</author></authors></contributors><titles><title>ATriterpenoidInhibitedHormone-InducedAdipocyteDifferentiationandAlleviatedDexamethasone-InducedInsulinResistancein3T3-L1adipocytes</title><secondary-title>NaturalProductsandBioprospecting</secondary-title></titles><periodical><full-title>NaturalProductsandBioprospecting</full-title></periodical><pages>159-166</pages><volume>5</volume><number>3</number><dates><year>2015</year><pub-dates><date>2015/06/01</date></pub-dates></dates><isbn>2192-2209</isbn><urls><related-urls><url>/10.1007/s13659-015-0063-5</url></related-urls></urls><electronic-resource-num>10.1007/s13659-015-0063-5</electronic-resource-num></record></Cite></EndNote>[3]。此外，在神經(jīng)科學(xué)研究領(lǐng)域，Insulin（AbMole，M9194）同樣展現(xiàn)出重要的應(yīng)用價(jià)值。有研究表明，Insulin能夠通過血腦屏障，影響中樞神經(jīng)系統(tǒng)的功能，參與調(diào)節(jié)食欲、能量平衡以及認(rèn)知功能等過程。例如，通過腦室內(nèi)注射Insulin，可以觀察到動(dòng)物攝食量的顯著減少，這一發(fā)現(xiàn)為肥胖的研究提供了新的思路ADDINEN.CITEADDINEN.CITE.DATA[4]。同時(shí)，Insulin（Pig，AbMole，M9336）在神經(jīng)免疫反應(yīng)中也具有重要的功能。Insulin能抑制小膠質(zhì)細(xì)胞介導(dǎo)的神經(jīng)炎癥，保護(hù)神經(jīng)元免受應(yīng)激損傷ADDINEN.CITEADDINEN.CITE.DATA[5]。Insulin信號(hào)還可通過調(diào)節(jié)線粒體功能和多巴胺能神經(jīng)元的存活影響帕金森?。≒D）動(dòng)物模型的進(jìn)展ADDINEN.CITEADDINEN.CITE.DATA[6]。圖1Insulin參與的信號(hào)通路ADDINEN.CITE<EndNote><Cite><Author>Petersen</Author><Year>2018</Year><RecNum>1343</RecNum><DisplayText><styleface="superscript">[7]</style></DisplayText><record><rec-number>1343</rec-number><foreign-keys><keyapp="EN"db-id="f2td9w00a22awteprfrp9vaup9d9zwa9tdfr"timestamp="1762240249">1343</key></foreign-keys><ref-typename="JournalArticle">17</ref-type><contributors><authors><author>Petersen,MaxC</author><author>Shulman,GeraldI%JPhysiologicalreviews</author></authors></contributors><titles><title>Mechanismsofinsulinactionandinsulinresistance</title></titles><dates><year>2018</year></dates><urls></urls></record></Cite></EndNote>[7]范例詳解SciAdv.2025Jul25;11(30):eadi2370.中山大學(xué)的科研團(tuán)隊(duì)在上述論文中開發(fā)了一種誘導(dǎo)多能干細(xì)胞生成功能性乳腺樣細(xì)胞（MC）和乳腺類器官的方法。上述模型可用于模擬乳腺組織的發(fā)育過程和解析乳腺癌產(chǎn)生的分子機(jī)制。此外，實(shí)驗(yàn)人員通過上述模型還揭示了S100P是乳腺癌腫瘤發(fā)生的關(guān)鍵基因。由AbMole提供的Insulin（Human，AbMole，M9194）在上述實(shí)驗(yàn)中，作為培養(yǎng)基中重要的組成成分之一，維持乳腺相關(guān)細(xì)胞的存活、增殖和正常功能。在3D培養(yǎng)體系中Insulin（10μg/ml）還用于誘導(dǎo)iPSC-MCs形成乳腺樣類器官，保障類器官結(jié)構(gòu)形成與功能穩(wěn)定ADDINEN.CITEADDINEN.CITE.DATA[8]。圖2.ClinicalanalysisrevealsanassociationofS100PandBRCA1intumorigenesisADDINEN.CITEADDINEN.CITE.DATA[8].參考文獻(xiàn)及鳴謝ADDINEN.REFLIST[1]MaxC.Petersen,GeraldI.Shulman,MechanismsofInsulinActionandInsulinResistance,98(4)(2018)2133-2223.[2]A.Rossi,M.Eid,J.Dodgson,etal.,Invitrocharacterizationoftheeffectsofchronicinsulinstimulationinmouse3T3-L1andhumanSGBSadipocytes,Adipocyte9(1)(2020)415-426.[3]Ji-HuanQin,Jun-ZengMa,Xing-WeiYang,etal.,ATriterpenoidInhibitedHormone-InducedAdipocyteDifferentiationandAlleviatedDexamethasone-InducedInsulinResistancein3T3-L1adipocytes,NaturalProductsandBioprospecting5(3)(2015)159-166.[4]M.Dahiya,M.Yadav,C.Goyal,etal.,InsulinresistanceinAlzheimer'sdisease:signallingmechanismsandtherapeuticsstrategies,Inflammopharmacology33(4)(2025)1817-1831.[5]C.C.Huang,S.F.Tsai,S.C.Liu,etal.,InsulinMediatesLipopolysaccharide-InducedInflammatoryResponsesandOxidativeStressinB