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甲状腺功能亢进症患儿胰岛素抵抗和胰岛素受体变化
引用本文:何健峰,雷培芸,熊丰,邓蕾丽,杨锡强,程欣然,王栋刚,杨渝生. 甲状腺功能亢进症患儿胰岛素抵抗和胰岛素受体变化[J]. 现代医药卫生, 2003, 19(4): 380-382
作者姓名:何健峰  雷培芸  熊丰  邓蕾丽  杨锡强  程欣然  王栋刚  杨渝生
作者单位:重庆医科大学附属儿童医院,400014
摘    要:目的:探讨甲状腺功能亢进(甲亢)患儿糖代谢紊乱的特点及发生的可能机制。方法:用血糖仪和放射免疫方法检测29例甲亢患儿餐前、餐后60分钟、120分钟血糖和餐前、餐后60分钟胰岛素、C肽、胰高糖素、皮质醇及T3、T4、TSH、抗甲状腺球蛋白抗体(TGA)、抗甲状腺微粒体抗体(TMA)(其中10例糖耐量减低为甲亢1组,另19例糖耐量正常为甲亢2组),并与20例正常健康儿童进行比较。采用放射受体分析法对其中的14例甲亢患儿餐前、餐后60分钟进行了红细胞胰岛素受体的检测,以7名健康儿童作为对照。结果:29例甲亢患儿10例出现糖代谢紊乱,病程大于1年和小于1年糖代谢紊乱发生率为50%和9%(P<0.05)。甲亢1组餐后60分钟胰岛素、胰岛素/血糖、胰岛素/胰高糖素显著升高(P<0.05);红细胞膜高、低亲和力胰岛素受体数目餐前、餐后自身对照均明显下降(P<0.05);低亲和力胰岛素受体亲和力餐前、餐后自身对照明显升高(P<0.05)。结论:甲亢儿童存在糖代谢紊乱现象,表现为葡萄糖耐量低减和胰岛素抵抗,其发生与病程有关,病程较长,发生率较高。胰岛素靶细胞受体数目减少及亲和力的改变可能是甲亢糖代谢紊乱及胰岛素抵抗的重要原因。

关 键 词:甲状腺功能亢进症 胰岛素抵抗 儿童 胰岛素受体 糖耐量减低
文章编号:1009-5519(2003)04-0380-03

Evaluation of glucose metabolism disorder in hyperthyroidism children: insulin resistance and abnormal insulin receptors.
HeJianfeng,LeiPeiyun,XONGFeng,DengLeili,Yang Xiqiang. Cheng Xinran,Wang Donggang,YangYushen,Childern' s Hospital,Chongqing University of Medical Sciences,Chongqing. Evaluation of glucose metabolism disorder in hyperthyroidism children: insulin resistance and abnormal insulin receptors.[J]. JOURNAL OF MODERN MEDICINE & HEALTH, 2003, 19(4): 380-382
Authors:HeJianfeng  LeiPeiyun  XONGFeng  DengLeili  Yang Xiqiang. Cheng Xinran  Wang Donggang  YangYushen  Childern' s Hospital  Chongqing University of Medical Sciences  Chongqing
Affiliation:HeJianfeng,LeiPeiyun,XONGFeng,DengLeili,Yang Xiqiang. Cheng Xinran,Wang Donggang,YangYushen,Childern' s Hospital,Chongqing University of Medical Sciences,Chongqing 400014
Abstract:Objective: The purpose of this study was to evaluate features and underlying pathogenesis of glucose metabolism disorder in pediatric patients with hyperthyroidism. Methods: Fasting, post - prandial 60 minute and post - prandial 120 minute blood glucose were measured using SUPER GLUCOCARDTM glucose meter. The levels of insulin, c - peptide, glucagon, cortisol in fasting and post - prandial 60 minute and T3, T4, TSH, anti - thyroglobulin antibody (TGA), anti - microsomalantibody(TMA) in fasting were measured using radio - immunity assay(RIA) in 29 patients with hyperthyroidism were divied into two groups : group one included 10 cases impaired glucose tolerance and group two consisted of 19 cases with normal glucose tolerance. 20 nomal age - matched children served as controls. In addition, erythrocyte fasting and post - prandial 60 minute insulin receptor of 14 with hyperthyroidism and 7 normal age - matched controls were measured using insulin radioreceptor assay. Results: Abnormal glucose metabolism were found in 10 of 29 patients with hyperthyroidism. Incidence of glycometabolic disorder was 50 % in patients with more than one year course compared with 9% incases withless than one year disease course(P<0.05) . In hyperthyroidism with glycometabolic disorder ( group 1) . Levels of glucose, insulin, insulin/glucose, insulin/glucagon in post-prandial 60 minute were significantly increasing; Numbers of fasting insulin receptor of tall and low affinity in erythrocyte membrane were lower than post ?prandial insulin receptor (P < 0.05) ; Avidity of post - prandial insulin receptor of low affinity in erythrocyte membrane are lower than it of fasting insulin receptor (P < 0.05). Conclusions: Glycometabolic disorder with impaired glucose tolerance and insulin resistance are present in patients with hyperthyroidism. The longer was course of the disease, the higher was incidence of gly-cometabolism. insulin receptor on Target cells decreased the numbers and altered affinity might play important roles in the mechanisms of glycometabolic disorder and insulin resistance in children with hyperthyroidism.
Keywords:hyperthyroidism impaired glucose tolerance insulin receptor insulin resistance
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