2型糖尿病患者FAT/CD36基因启动子区-3489C/T和密码子区478C/T多态性研究
曾蓉,严新民,宋滇平,高建梅 曾蓉、宋滇平,昆明医学院第一附属医院糖尿病科,650031;严新民、高建梅,云南省第一人民医院基础医学研究所
摘要:目的 探讨FAT/CD36脂肪酸转位酶基因启动子区-3489C/T和密码子区478C/T多态性与2型糖尿病(T2DM)的相关性。方法 运用聚合酶链反应-限制性片段长度多态性技术对196例T2DM患者和120例正常对照者的-3489C/T与478C/T多态性进行检测,并比较各组间基因型频率和等位基因频率以及相关临床资料。结果 (1)所有研究对象均无一例存在FAT/CD36基因启动子区478C→T突变,基因型均表现为478CC之纯合子,478CC和478TT等位基因频率分别为1和0。(2)T2DM组和正常对照组的-3489C/T多态性基因型和等位基因频率比较差异无统计学意义,P值分别为0.682和0.683。结论 昆明地区的汉族人中FAT/CD36基因的启动子区-3489C/T和密码子区478位C/T多态性与昆明地区汉族人群2型糖尿病的发生无显著相关关系。
糖尿病,2型;态现象,遗传;脂肪酸转位酶
文献标引:曾蓉,严新民,宋滇平,高建梅.2型糖尿病患者FAT/CD36基因启动子区-3489C/T和密码子区478C/T多态性研究.中华临床医师杂志(电子版),2008,2(3):276-283.
参考文献
[1] Corpeleijn E, van der Kallen CJ, Kruijshoop M, et al. Direct association of a promoter polymorphism in the CD36/FAT fatty acid transporter gene with Type 2 diabetes mellitus and insulin resistance.Diabet Med,2006,23(8):907-911.[PubMed][2] Tanaka T, Nakata T, Oka T, et al.Defect in human myocardial long-chain fatty acid uptake is caused by FAT/CD36 mutations.J Lipid Res,2001,42(5):751-759.[PubMed]
[3] 高磊,鲍羿,洪斌.B类清道夫受体CD36的研究进展.医学分子生物学杂志,2006,3(1):61-64.
[4] Bezaire V, Bruce CR, Heigenhauser GJ, et al.Identification of fatty acid translocase on human skeletal muscle mitochondrial membranes:essential role in fatty acid oxidation.Am J Physiol Endocrinol Metab,2006,290(3):E509-515.[PubMed]
[5] Luiken JJ, Dyck DJ, Han XX, et al. Insulin induces the translocation of the fatty acid transporter FAT/CD36 to the plasma membrane.Am J Physiol Endocrinol Metab,2002,282(2):E491-495.[PubMed]
[6] Wilmsen HM, Ciaraldi TP, Carter L, et al.Thiazolidinediones upregulate impaired fatty acid uptake in skeletal muscle of type 2 diabetic subjects.Am J Physiol Endocrinol Metab,2003,285(2):E354-362.[PubMed]
[7] Corpeleijn E,Saris WH,Jansen EH,et al.Postprandial interleukin 6 release from skeletal muscle in men with impaired glucose tolerance can be reduced by weight loss.J Clin Endocrinol Metab,2005,90(10):5819-5824.[PubMed]

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