甲状腺疾病患者小腿肌肉的生物能量损伤：31P MRS 研究。
Bio-energetic impairment in human calf muscle in thyroid disorders: a 31P MRS study.
机构信息
NMR Research Centre, INMAS, DRDO, Timarpur, Delhi, India.
出版信息
Magn Reson Imaging. 2010 Jun;28(5):683-9. doi: 10.1016/j.mri.2010.01.006. Epub 2010 Mar 23.
Mitochondrial metabolism particularly oxidative phosphorylation is greatly influenced by thyroid hormones. Earlier studies have described neuromuscular symptoms as well as impaired muscle metabolism in hypothyroid and hyperthyroid patients. In this study, we intend to look in to the muscle bioenergetics including phosphocreatine recovery kinetics based oxidative metabolism in thyroid dysfunction using in vivo (31)P nuclear magnetic resonance spectroscopy (MRS). (31)P MRS was carried out at resting state on 32 hypothyroid, 10 hyperthyroid patients and 25 control subjects. Nine out of 32 hypothyroid patients and 17 out of 25 control subjects under went exercise protocol for oxidative metabolism study and performed plantar flexion exercise while lying supine in 1.5 T magnetic resonance scanner using custom built exercise device. MRS measurements of inorganic phosphate (Pi), phosphocreatine (PCr), phosphodiesters (PDE) and adenosine triphosphate (ATP) of the calf muscle were acquired during rest, exercise and recovery phase. PCr recovery rate constant (k(PCr)) and oxidative capacity were calculated by monoexponential fit of PCr versus time (t) at the beginning of recovery. During resting condition in hypothyroid patients, PCr/Pi ratio was reduced whereas PDE/ATP and Pi/ATP were increased. However, in case of hyperthyroidism, an increased PCr/Pi ratio and reduced PDE/ATP and Pi/ATP were observed. The results confirmed differential energy status of the muscle due to increased or decreased levels of thyroid hormone. Our results also demonstrate reduced oxidative metabolism in hypothyroid patients based on PCr recovery kinetics. PCr recovery kinetics study after exercise revealed decreased PCr recovery rate constant (k(PCr)) in hypothyroid patients compared to controls that resulted in decrease in oxidative capacity of muscle by 50% in hypothyroids. These findings are consistent with a defect of high energy phosphate mitochondrial metabolism in thyroid dysfunction.
线粒体代谢，特别是氧化磷酸化，受甲状腺激素的影响很大。早期的研究已经描述了甲状腺功能减退症和甲状腺功能亢进症患者的神经肌肉症状以及肌肉代谢受损。在这项研究中，我们旨在通过体内（31）P 磁共振波谱（MRS）观察甲状腺功能障碍患者的肌肉生物能量学，包括磷酸肌酸恢复动力学和氧化代谢。（31）P MRS 在 32 名甲状腺功能减退症患者、10 名甲状腺功能亢进症患者和 25 名对照组患者的静息状态下进行。在 32 名甲状腺功能减退症患者中，有 9 名和 25 名对照组患者中的 17 名进行了氧化代谢研究的运动方案，在 1.5T 磁共振扫描仪中仰卧位使用定制的运动装置进行足底屈肌运动。在休息、运动和恢复阶段，采集小腿肌肉的无机磷酸盐（Pi）、磷酸肌酸（PCr）、磷酸二酯（PDE）和三磷酸腺苷（ATP）的 MRS 测量值。通过在恢复开始时 PCr 与时间（t）的单指数拟合计算 PCr 恢复速率常数（k（PCr））和氧化能力。在甲状腺功能减退症患者的休息状态下，PCr/Pi 比值降低，而 PDE/ATP 和 Pi/ATP 增加。然而，在甲状腺功能亢进症中，观察到 PCr/Pi 比值增加，PDE/ATP 和 Pi/ATP 减少。结果证实了由于甲状腺激素水平的增加或减少，肌肉的能量状态存在差异。我们的结果还表明，基于 PCr 恢复动力学，甲状腺功能减退症患者的氧化代谢减少。运动后的 PCr 恢复动力学研究显示，与对照组相比，甲状腺功能减退症患者的 PCr 恢复速率常数（k（PCr））降低，导致甲状腺功能减退症患者的肌肉氧化能力降低 50%。这些发现与甲状腺功能障碍中线粒体高能磷酸盐代谢的缺陷一致。
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