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氧化应激在2型糖尿病发生发展中的作用机制 被引量:20

Mechanism of oxidative stress in the occurrence and development of type 2 diabetes mellitus
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摘要 随着对2型糖尿病(type 2 diabetes mellitus,T2DM)病理生理机制的深入探索,众多研究发现氧化应激在其发生发展的过程中扮演了不可忽视的角色。T2DM发生的最初启动因素是胰岛β细胞功能缺陷或胰岛素抵抗(insulin resistance,IR)。慢性高血糖会使机体活性氧簇(reactive oxygen species,ROS)生成过高并超出抗氧化防御系统的防御能力,导致氧化应激(oxidative stress,OS)。而OS通过一系列信号通路对机体产生影响,使胰岛β细胞功能受损以及造成IR等,最终造成T2DM。另外,遗传、环境、年龄、生活方式等因素也可能导致T2DM的发生。本研究对OS与T2DM的发病机制进行综述,并讨论未来可能的治疗手段。 With the in-depth exploration of the pathophysiological mechanism of type 2 diabetes mellitus(T2DM),many studies have found that oxidative stress plays an important role in its occurrence and development.The initial initiating factor of T2DM is the defect of pancreaticβ-cell function or insulin resistance(IR).During the course of the disease,chronic hyperglycemia will cause the body to generate too much reactive oxygen species(ROS)and exceed the defense capabilities of the antioxidant defense system,leading to oxidative stress(OS).OS has an impact on the body through a series of signal pathways,impairing the function of pancreaticβ-cells and causing IR,and ultimately T2DM.In addition,factors such as genetics,environment,age,and lifestyle may also lead to the occurrence of T2DM.Therefore,this article reviews the pathogenesis of OS and T2DM,and discusses possible future treatments.
作者 魏书瑶 冯珊珊 马菲菲 哈小琴 WEI Shuyao;FENG Shanshan;MA Feifei;HA Xiaoqin(Gansu University of Chinese Traditional Medicine,Lanzhou 730030,China;Gansu Agricultural University;The 940th Hospital of Joint Logistic Support Force of PLA)
出处 《西北国防医学杂志》 CAS 2021年第6期557-562,共6页 Medical Journal of National Defending Forces in Northwest China
基金 国家自然科学基金资助项目(81273568)。
关键词 2型糖尿病 氧化应激 胰岛素抵抗 type 2 diabetes mellitus oxidative stress insulin resistance
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  • 1Cossarizza A, Ferraresi R, Troiano L, Roat E, Gibellini L,Bertoncelli L, Nasi M, Pinti M. Simultaneous analysis of reactiveoxygen species and reduced glutathione content in living cells bypolychromatic flow cytometry. Nat Protoc 2009; 4: 1790-1797[PMID: 20010930 DOI: 10.1038/nprot.2009.189].
  • 2Turrens JF, Boveris A. Generation of superoxide anion by theNADH dehydrogenase of bovine heart mitochondria. Biochem J1980; 191: 421-427 [PMID: 6263247].
  • 3Sies H. Oxidative stress: oxidants and antioxidants. Exp Physiol1997; 82: 291-295 [PMID: 9129943].
  • 4Freeman BA, Crapo JD. Biology of disease: free radicals andtissue injury. Lab Invest 1982; 47: 412-426 [PMID: 6290784].
  • 5Slater TF. Free-radical mechanisms in tissue injury. Biochem J1984; 222: 1-15 [PMID: 6383353].
  • 6Dobrian AD, Davies MJ, Schriver SD, Lauterio TJ, Prewitt RL.Oxidative stress in a rat model of obesity-induced hypertension.Hypertension 2001; 37: 554-560 [PMID: 11230334 DOI: 10.1161/01.HYP.37.2.554].
  • 7Vincent HK, Taylor AG. Biomarkers and potential mechanisms ofobesity-induced oxidant stress in humans. Int J Obes (Lond) 2006;30: 400-418 [PMID: 16302012 DOI: 10.1038/sj.ijo.0803177].
  • 8Furukawa S, Fujita T, Shimabukuro M, Iwaki M, Yamada Y,Nakajima Y, Nakayama O, Makishima M, Matsuda M, ShimomuraI. Increased oxidative stress in obesity and its impact on metabolicsyndrome. J Clin Invest 2004; 114: 1752-1761 [PMID: 15599400].
  • 9Houstis N, Rosen ED, Lander ES. Reactive oxygen species havea causal role in multiple forms of insulin resistance. Nature 2006;440: 944-948 [PMID: 16612386 DOI: 10.1038/nature04634].
  • 10Ogihara T, Asano T, Ando K, Chiba Y, Sakoda H, Anai M,Shojima N, Ono H, Onishi Y, Fujishiro M, Katagiri H, FukushimaY, Kikuchi M, Noguchi N, Aburatani H, Komuro I, Fujita T.Angiotensin II-induced insulin resistance is associated withenhanced insulin signaling. Hypertension 2002; 40: 872-879[PMID: 12468572 DOI: 10.1161/01.HYP.0000040262.48405.A8].

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