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亚临床甲状腺功能减退症会影响线粒体功能。

Subclinical hypothyroidism affects mitochondrial function.

机构信息

Department of Internal Medicine, Faculty of Health Sciences, University of Copenhagen, Denmark.

出版信息

Horm Metab Res. 2010 May;42(5):324-7. doi: 10.1055/s-0030-1248261. Epub 2010 Feb 22.

DOI:10.1055/s-0030-1248261
PMID:20178065
Abstract

The aim of the present study was to examine mitochondrial function in cells from persons with subclinical hypothyroidism and euthyroid controls. The participating persons were examined clinically and had basal oxygen consumption (VO(2)) determined. The concentrations of thyroid hormones and thyrotropine stimulating hormone were determined, and mitochondrial function in isolated mononuclear blood cells was examined by enzymatic methods [citrate synthase activity (CS)] and by flow cytometry (mitochondrial membrane potential by TMRM fluorescence and mitochondrial mass by MTG fluorescence). The ratio of T(4)/T(3) was lowered in subclinical hypothyroidism patients compared to controls (2.5+/-0.5 vs. 2.9+/-0.4, p=0.005). VO(2) was increased in persons with subclinical hypothyroidism compared to controls (adolescents: 134+/-27 ml O(2)/minm(2) vs. 119+/-27 ml O(2)/minm(2), p=0.006, adults: 139+/-14 ml O(2)/minm(2) vs. 121+/-17 ml O(2)/minm(2), p=0.001). The mitochondrial function, represented by citrate synthase activity, MTG, and TMRM fluorescence were all increased (CS in subclinical hypothyroidism vs. controls: 0.074+/-0.044 nmol/mgmin vs. 0.056+/-0.021 nmol/mgmin, p=0.005; MTG fluorescence in subclinical hypothyroidism vs. controls: 7,482+/-1,733 a.u. vs. 6,391+/-2,171 a.u., p=0.027; TMRM fluorescence in subclinical hypothyroidism vs. controls: 13,449+/-3,807 a.u. vs. 11,733+/-4,473 a.u, p=0.04). Our results indicate an increased mitochondrial stimulation, eventually caused by increased deiodination of T(4) to intracellular bioactive iodothyronines in adults and adolescents with subclinical hypothyroidism.

摘要

本研究旨在研究亚临床甲状腺功能减退症患者和甲状腺功能正常对照者的细胞中线粒体功能。参与研究的人员进行了临床检查,并测定了基础耗氧量(VO2)。测定了甲状腺激素和促甲状腺激素的浓度,并通过酶法[柠檬酸合酶活性(CS)]和流式细胞术(TMRM 荧光的线粒体膜电位和 MTG 荧光的线粒体质量)检测分离的单核血细胞中的线粒体功能。与对照组相比,亚临床甲状腺功能减退症患者的 T4/T3 比值降低(2.5+/-0.5 对 2.9+/-0.4,p=0.005)。与对照组相比,亚临床甲状腺功能减退症患者的 VO2 增加(青少年:134+/-27 ml O2/minm2 对 119+/-27 ml O2/minm2,p=0.006,成人:139+/-14 ml O2/minm2 对 121+/-17 ml O2/minm2,p=0.001)。线粒体功能,以柠檬酸合酶活性、MTG 和 TMRM 荧光表示,均增加(亚临床甲状腺功能减退症患者的 CS 与对照组相比:0.074+/-0.044 nmol/mgmin 对 0.056+/-0.021 nmol/mgmin,p=0.005;MTG 荧光在亚临床甲状腺功能减退症患者与对照组相比:7482+/-1733 a.u. 对 6391+/-2171 a.u.,p=0.027;TMRM 荧光在亚临床甲状腺功能减退症患者与对照组相比:13449+/-3807 a.u. 对 11733+/-4473 a.u.,p=0.04)。我们的结果表明,亚临床甲状腺功能减退症的成年人和青少年的 T4 向细胞内生物活性碘甲状腺素的脱碘作用增加,最终导致线粒体刺激增加。

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