Everts M E
Institute of Physiology, University of Aarbus, Denmark.
Acta Physiol Scand. 1996 Mar;156(3):325-33. doi: 10.1046/j.1365-201X.1996.203000.x.
Skeletal muscle is one of the major target organs for thyroid hormone. The muscles most commonly affected are those used during prolonged effort (slow-twitch muscles). One of the major clinical features is the shortening of the Achilles-tendon reflex time in hyperthyroidism and its prolongation in hypothyroidism. Most of the peripheral effects of the thyroid hormones can be ascribed to the action of triiodothyronine (T2), which is produced by de-iodination of thyroxine (T4) in liver and kidney. From the plasma, T3 is actively transported into skeletal muscle. The Ca2+ ATPase in skeletal muscle is responsible for removal of Ca2+ ions from the cytosol into the sarcoplasmic reticulum (SR) during relaxation, and the Na+, K+ ATPase in the plasma membrane is responsible for restoration of the membrane potential after excitation. The concentrations of Ca2+ ATPase and Na+, K+ ATPase in rat skeletal muscle have been shown to increase four- and 10-fold, respectively, in the transition from the hypothyroid to the hyperthyroid state. In humans, a linear correlation between the Na+, K+ ATPase concentration of skeletal muscle and the free T4 index was established. Significant effects of T3 on Ca2+ ATPase and Na+, K+ ATPase can be detected 24 h after a single injection. These effects are mediated by increased production of mRNA for the respective proteins, initiated by binding of T3 to nuclear receptors. Passive fluxes of Ca2+, Na+ and K+ also show a significant rise after T3 treatment. The increase in passive fluxes of Na+ and K+ can be detected before the rise in the concentration of Na+, K+ ATPase, suggesting that T3. In addition to its nuclear effects, may have a direct effect on the plasma membrane. Apart from their significance for muscle function in thyroid disease, the changes in Ca2+ ATPase and Na+, K+ ATPase will be important in other conditions where T3 and T4 levels show dramatic changes, i.e. during postnatal development, starvation and undernutrition, as well as in non-thyroidal illness (low-T3 syndrome).
骨骼肌是甲状腺激素的主要靶器官之一。最常受影响的肌肉是长时间运动时使用的肌肉（慢肌纤维）。主要临床特征之一是甲状腺功能亢进时跟腱反射时间缩短，甲状腺功能减退时跟腱反射时间延长。甲状腺激素的大多数外周效应可归因于三碘甲状腺原氨酸（T3）的作用，T3是由肝脏和肾脏中的甲状腺素（T4）脱碘产生的。T3从血浆中被主动转运到骨骼肌中。骨骼肌中的Ca2+ATP酶负责在舒张期将Ca2+离子从细胞质转运到肌浆网（SR）中，质膜中的Na+、K+ATP酶负责在兴奋后恢复膜电位。从甲状腺功能减退状态转变为甲状腺功能亢进状态时，大鼠骨骼肌中Ca2+ATP酶和Na+、K+ATP酶的浓度分别增加了4倍和10倍。在人类中，骨骼肌中Na+、K+ATP酶浓度与游离T4指数之间建立了线性关系。单次注射T3后24小时即可检测到T3对Ca2+ATP酶和Na+、K+ATP酶的显著影响。这些影响是由T3与核受体结合引发的相应蛋白质mRNA产生增加介导的。T3治疗后，Ca2+、Na+和K+的被动通量也显著增加。在Na+、K+ATP酶浓度升高之前就能检测到Na+和K+被动通量的增加，这表明T3除了其核效应外，可能对质膜有直接作用。除了对甲状腺疾病中肌肉功能的重要性外，Ca2+ATP酶和Na+、K+ATP酶的变化在其他T3和T4水平发生显著变化的情况下也很重要，即在出生后发育、饥饿和营养不良期间，以及在非甲状腺疾病（低T3综合征）中。
