补体c1q/肿瘤坏死因子相关蛋白9在妊娠期糖尿病发病中的作用分析
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  • 作者:钟敏 ; 朱艳宾 ; 黄为群 ; 李岩 ; 陆丽
  • 关键词:妊娠期糖尿病 ; 补体c1q/肿瘤坏死因子相关蛋白 ; 胰岛素抵抗
  • 中文刊名:ZFYB
  • 英文刊名:Maternal and Child Health Care of China
  • 机构:深圳市龙华区人民医院产科;南方医科大学附属深圳医院产科;
  • 出版日期:2019-07-15
  • 出版单位:中国妇幼保健
  • 年:2019
  • 期:v.34
  • 基金:深圳市龙华新区科技创新资金项目(20160831A1030159)
  • 语种:中文;
  • 页:ZFYB201914057
  • 页数:3
  • CN:14
  • ISSN:22-1127/R
  • 分类号:188-190
摘要
目的分析补体c1q/肿瘤坏死因子相关蛋白9 (C1QTNF9)在妊娠期糖尿病发病中的作用。方法选取2016年9月-2017年8月在深圳市龙华区人民医院产科住院分娩的20例足月单胎GDM孕妇为研究组,同期产检并住院剖宫产的20例足月单胎糖耐量正常孕妇为对照组。收集临床资料,检测空腹血糖及胰岛素水平,应用双抗体夹心酶标免疫分析法检测血清C1QTNF9水平,检测胎盘组织中C1QTNF9蛋白和m RNA表达水平,分析血清C1QTNF9与胰岛素抵抗指数及糖代谢指标的相关性。结果两组孕妇妊娠前BMI、分娩时BMI、孕期体质量增长、空腹血糖及空腹胰岛素水平、HOMA-IR、血清C1QTNF9和肿瘤坏死因子-α(TNF-α)水平比较,差异均有统计学意义(均P<0. 05)。两组胎盘组织中C1QTNF9 m RNA及蛋白表达水平比较差异均有统计学意义(均P>0. 05)。血清C1QTNF9水平与血清TNF-α水平、分娩期BMI、HOMA-IR、空腹胰岛素水平均呈负相关。结论 C1QTNF9表达于孕妇血清及胎盘组织中,其表达水平降低可引起胰岛素抵抗增强,导致妊娠期糖尿病的发生。
        
引文
[1]Homko CJ.New recommendations for the diagnosis of diabetes in pregnancy[J].Curr Diab Rep,2011,11(1):1-3.
    [2]American Diabetes Association.Diagonosis and classification of diabetes mellitus[J].Diabetes Care,2011,40(34):62-69.
    [3]郝宝珺,沈洁,万亨,等.广州天河区妊娠期糖尿病发病率回顾性调查[J].中国糖尿病杂志,2014,6(7):620-621.
    [4]徐湘,朱晓巍,蒋艳敏,等.2 748例住院孕妇妊娠期糖尿病发病率及危险因素的研究[J].南京医科大学学报(自然科学版),2015,60(5):695-698.
    [5]Galic S,Oakhill JS,Steinberg GR.Adipose tissue as an endocrine organ[J].Mol Cell Endocrinol,2010,316(2):129-139.
    [6]Wong GW,Krawczyk SA,Kitidis-Mitrokostas C,et al.Molecular,biochemical and functional characterizations of C1q/TNF family members:adipose-tissue-selective expression patterns,regulation by PPAR-gamma agonist,cysteine-mediated oligomerizations,combinatorial associations and metabolic functions[J].Biochem J,2008,416(2):161-177.
    [7]American Diabetes Association.Standards of medical care in diabetes-2011[J].Diabetes Care,2011,34(Suppl 1):S11-S61.
    [8]Sokup A,Ruszkow Ska-Cliastek B,Goralczyk K,et al.Insulin resistance as estimated by homeostatic method at diagnosis of gestational diabetes:estimation of disease severity and therapeutic needs in a population-based study[J].BMC Endocr Disord,2013,13(12):21-30.
    [9]Wong GW,Krawczyk SA,Kitidis-Mitrokostas C,et al.Identification and characterization of CTRP9,a novel secreted glycoprotein,from adipose tissue that reduces serum glucose in mice and forms heterotrimers with adiponectin[J].FASEB J,2009,23(1):241-258.
    [10]王欣荣,吕伯昌,李海燕,等.血清补体C1q肿瘤坏死因子相关蛋白3、补体C1q肿瘤坏死因子相关蛋白9水平对糖尿病视网膜病变患者的影响及相关性研究[J].中国医药导报,2015,12(26):8-11.
    [11]Hwang YC,Wooo HS,Parks W,et al.Association of serum C1q/TNF-αelated protein-9(CTRP9)concentration with visceral adiposity and metabolic syndrome in humans[J].Int J Obes(Lond),2014,38(9):1207-1212.
    [12]Kambara T,Ohashi K,Shibata R,et al.CTRP9 protein protects against myocardial injury following ischemia-reperfusion through AMP-activated protein kinase(AMPK)-dependent mechanism[J].J Biol Chem,2012,287(23):18965-18973.
    [13]Ma K,Cabrero A,Saha PK,et al.Increased beta-oxidation but no insulin resistance or glucose intolerance in mice lacking adiponectin[J].J Biol Chem,2002,277(38):34658-34661.
    [14]Zhikui W,Xia L,Pia S,et al.Targeted deletion of C1q/TNF-related protein 9 increases food intake decreases insulin sensitivity and promotes hepatic steatosis in mice[J].Am J Physiol Endocrinol Metab,2014,30(67):E779-E790.
    [15]Peterson JM,Weiz,Seldinm M,et al.CTRP9 transgenic Mice are protected from diet-induced obesity and metabolic dysfunction[J].Am J Physiol Regul Integr Comp Physiol,2013,305(5):522-533.
    [16]Su H,Yuan Y,Wang XM,et al.Inhibition of CTRP9,a novel and cardiac-abundantly expressed cell survival molecule by TNF-alpha initiated oxidative signaling contributes to exacerbated cardiac injury in diabetic mice[J].Basic Res Cardiol,2013,108(1):315.
    [17]Huang Z,Cui T,Liu J,et al.Characterization of the expression of CTRP9:a paralog of adiponectin[J].Tsinghua Sci Technol,2008,13(4):492-499.

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