[1]李影,张真稳.线粒体损伤与糖尿病发病的相关机制[J].国际内分泌代谢杂志,2014,(04):271-273，280.[doi:10.3760/cma.j.issn.1673-4157.2014.04.016]
　Li Ying,Zhang Zhenwen..Relationship between mitochondrial damage and diabetes mellitus[J].International Journal of Endocrinology and Metabolism,2014,(04):271-273，280.[doi:10.3760/cma.j.issn.1673-4157.2014.04.016]
点击复制

线粒体损伤与糖尿病发病的相关机制()
分享到：

《国际内分泌代谢杂志》[ISSN:1673-4157/CN:12-1383/R]

卷:
期数:
2014年04期
页码:
271-273，280
栏目:
综述
出版日期:
2014-08-31

文章信息/Info

Title:
Relationship between mitochondrial damage and diabetes mellitus
作者:
李影; 张真稳
作者单位：225001　扬州，江苏省苏北人民医院内分泌科 　　
Author(s):
Li Ying; Zhang Zhenwen.
Department of Endocrinology，Subei People′s Hospital of Jiangsu Province，Yangzhou 225001，China Corresponding author：Zhang Zhenwen，Email：yzzzw@medmail.com.cn
关键词:
线粒体; 糖尿病; 活性氧簇; 解耦联蛋白2; 自噬
Keywords:
Mitochondria; Diabetes mellitus; Reactive oxygen species; Uncoupling protein 2; Autophagy
DOI:
10.3760/cma.j.issn.1673-4157.2014.04.016
摘要:
线粒体是机体代谢和能量合成的重要场所，其功能损伤与糖尿病的发病有密切联系。线粒体跨膜电位超极化、解耦联蛋白2表达异常、线粒体自噬障碍引起线粒体功能或结构受损，导致活性氧簇的产生过多，加重胰岛素抵抗。线粒体自身甲状腺激素受体活性对胰腺转录因子的表达也有调节作用，间接影响胰岛素的分泌水平。同时，线粒体基因不同位点的变异与糖尿病发病易感性相关。了解线粒体损伤与糖尿病发病的相关机制将为糖尿病的治疗提供新的思路。
Abstract:
Mitochondria is an important place of metabolism and energy synthesis. Dysfunction of mitochondrial is closely related to diabetes. Excessive expression of reactive oxygen species（ROS） ， caused by the hyperpolarization of mitochondrial transmembrane potential，the abnormal expression of uncoupling protein 2 and impairment of autophagy which causes mitochondrial dysfunction and structural damage，accelerates the progress of insulin resistance. Mitochondria expresses have their own thyroid hormone receptors，which can modulate the expression of pancreatic transcription factors and affect the secretion of insulin indirectly. Meanwhile，the mutation of mitochondrial gene is associated with susceptibility of diabetes. Understanding the relationship between mitochondrial damage and diabetes will provide new ideas for the treatment of diabetes.

参考文献/References:

　[1]　Wallace DC，Fan W.The pathophysiology of mitochondrial disease as modeled in the mouse[J].Genes Dev，2009，23（15）：1714-1736. 　
[2]　Boesch P，Weber-Lotfi F，Ibrahim N，et al.DNA repair in organelles：Pathways，organization，regulation，relevance in disease and aging[J].Biochim Biophys Acta，2011，1813（1）：186-200. 　
[3]　Kizhakekuttu TJ，Wang J，Dharmashankar K，et al.Adverse alter-ations in mitochondrial function contribute to type 2 diabetes mellitus-related endothelial dysfunction in humans[J].Arterioscler Thromb Vasc Biol，2012，32（10）：2531-2539. 　
[4]　Grama CN，Suryanarayana P，Patil MA，et al.Efficacy of biodegr- adable curcumin nanoparticles in delaying cataract in diabetic rat model[J].PLoS One，2013，8：e78217. 　
[5]　Wang C H，Wang C C，Huang H C，et al.Mitochondrial dysfunction leads to impairment of insulin sensitivity and adiponectin secre-tion in adipocytes[J].FEBS J，2013，280（4）：1039-1050. 　
[6]　Taheripak G，Bakhtiyari S，Rajabibazl M，et al.Protein tyrosine phosphatase 1B inhibition ameliorates palmitate-induced mito-chondrial dysfunction and apoptosis in skeletal muscle cells[J].Free Radic Biol Med，2013，65：1435-1446. 　
[7]　Widlansky ME，Gutterman D D.Regulation of endothelial function by mitochondrial reactive oxygen species[J].Antioxid Redox Signal，2011，15（6）：1517-1530. 　
[8]　Shimasaki Y，Pan N，Messina LM，et al.Uncoupling protein 2 impacts endothelial phenotype via p53-mediated control of mitochondrial dynamics[J].Circ Res，2013，113（7）：891-901. 　
[9]　Robbins D，Zhao Y.New aspects of mitochondrial uncoupling proteins（UCPs） and their roles in tumorigenesis[J].Int J Mol Sci，2011，12（8）：5285-5293.
[10]　Bertrand C，Blanchet E，Pessemesse L，et al.Mice lacking the p43 mitochondrial T3 receptor become glucose intolerant and insulin resistant during aging[J].PLoS One，2013，8：e75111.
[11]　Pessemesse L，Schlernitzauer A，Sar C，et al.Depletion of the p43 mitochondrial T3 receptor in mice affects skeletal muscle development and activity[J].FASEB J，2012，26（2）：748-756.
[12]　Aguayo-Mazzucato C，Koh A，El Khattabi I，et al.Mafa expression enhances glucose-responsive insulin secretion in neonatal rat beta cells[J].Diabetologia，2011，54（3）：583-593.
[13]　Kondo T，El Khattabi I，Nishimura W，et al.p38 MAPK is a major regulator of MafA protein stability under oxidative stress[J].Mol Endocrinol，2009，23（8）：1281-1290.
[14]　Aguayo-Mazzucato C，Zavacki A M，Marinelarena A，et al. Thyroid hormone promotes postnatal rat pancreatic β-cell development and glucose-responsive insulin secretion through MAFA[J].Diabetes，2013，62（5）：1569-1580.
[15]　Park KS，Chan JC，Chuang LM，et al.A mitochondrial DNA variant at position 16189 is associated with type 2 diabetes mellitus in Asians[J].Diabetologia，2008，51（4）：602-608.
[16]　Liou CW，Chen JB，Tiao MM，et al.Mitochondrial DNA coding and control region variants as genetic risk factors for type 2 diabetes[J]. Diabetes，2012，61（10）：2642-2651.
[17]　Jung HS，Lee MS.Role of autophagy in diabetes and mito-chondria[J].Ann N Y Acad Sci，2010，1201：79-83.
[18]　Ebato C，Uchida T，Arakawa M，et al.Autophagy is important in islet homeostasis and compensatory increase of beta cell mass in response to high-fat diet[J].Cell Metab，2008，8（4）：325-332.
[19]　Marselli L，Bugliani M，Suleiman M，et al.β-Cell inflammation in human type 2 diabetes and the role of autophagy[J].Diabetes Obes Metab，2013，15（Suppl 3）：130-136.
[20]　van Tienen FH，Praet SF，de Feyter HM，et al.Physical activity is the key determinant of skeletal muscle mitochondrial function in type 2 diabetes[J].J Clin Endocrinol Metab，2012，97（9）：3261-3269.
[21]　Gauthier BR，Wiederkehr A，Baquié M，et al.PDX1 deficiency causes mitochondrial dysfunction and defective insulin secretion through TFAM suppression[J].Cell Metab，2009，10（2）：110-118.

相似文献/References:

[1]郑少雄.罗格列酮和心血管风险——近期文献解读[J].国际内分泌代谢杂志,2007,(04):231.
[2]凌厉,朱本章.胰岛素类似物安全性研究进展[J].国际内分泌代谢杂志,2007,(04):234.
[3]李颖,刘东方.餐后1小时血糖升高的意义及干预[J].国际内分泌代谢杂志,2007,(04):235.
[4]崔巍,施秉银.内质网应激介导β细胞生存/死亡的研究进展[J].国际内分泌代谢杂志,2007,(04):256.
[5]杨叶虹,胡仁明.SELDI-TOF-MS技术及其在糖尿病研究中的应用[J].国际内分泌代谢杂志,2007,(04):261.
[6]高妍.针对华人糖尿病特点优化降糖方案[J].国际内分泌代谢杂志,2007,(04):269.
[7]杨志霞,郭莹辉,杨永生,等.胰岛素泵和多次皮下注射治疗糖尿病的比较[J].国际内分泌代谢杂志,2007,(04):273.
[8]周建英,马向华.胃旁路术减肥同时改善糖代谢的机制[J].国际内分泌代谢杂志,2007,(04):285.
[9]李翠柳,朱大龙.破译肠道代谢信息,驱动治疗革新[J].国际内分泌代谢杂志,2014,(06):383.[doi:10.3760/cma.j.issn.1673-4157.2014.06.006]
　Li Cuiliu*,Zhu Dalong..Deciphering metabolic messages from the gut drives therapeutic innovation[J].International Journal of Endocrinology and Metabolism,2014,(04):383.[doi:10.3760/cma.j.issn.1673-4157.2014.06.006]
[10]袁捷 姜云生 杜彦丽 王肃.1型糖尿病对小鼠早孕时期子宫肌层结构和细胞增殖的影响[J].国际内分泌代谢杂志,2015,(01):6.[doi:10.3760/cma.j.issn.1673-4157.2015.01.002]
　Yuan JieJiang YunshengDu YanliWang Su.Effects of type 1 diabetes on the muscularis structure and cell proliferation of uterine in mice during early pregnancy[J].International Journal of Endocrinology and Metabolism,2015,(04):6.[doi:10.3760/cma.j.issn.1673-4157.2015.01.002]

备注/Memo

备注/Memo:
基金项目：国家卫生和计划生育委员会（W201309） 通信作者：张真稳，Email：yzzzw@medmail.com.cn
更新日期/Last Update: 2014-07-20