Effects of altered thyroid status on beta-adrenergic actions on skeletal muscle glycogen metabolism.
Effects of altered thyroid status on beta-adrenergic actions on skeletal muscle glycogen metabolism.
复制标题
甲状腺状态改变对骨骼肌糖原代谢的β-肾上腺素能作用的影响。
DOI：
10.1016/s0021-9258(17)39201-3
复制
发表时间：
1985
期刊：
影响因子：
--
通讯作者：
J. Exton
中科院分区：
文献类型：
--
作者：
D. T. Chu;H. Shikama;B. Khatra;J. Exton
采用大鼠后肢灌流标本，研究了甲状腺功能减退对大鼠骨骼肌糖原代谢的影响。丙基硫氧嘧啶治疗后3周，血清甲状腺素检测不到，肌糖原和葡萄糖-6-P下降。基础和肾上腺素刺激的磷酸化酶a和磷酸化酶B激酶活性也显著降低，肾上腺素刺激的cAMP积累和cAMP依赖性蛋白激酶活性也显著降低。相反，基础和肾上腺素刺激的糖原合酶I的活动显着较高，而葡萄糖-6-P的酶的Ka在甲状腺功能减退的动物较低。丙硫氧嘧啶治疗的大鼠也增加了磷蛋白磷酸酶对磷酸化酶和糖原合成酶的活性和磷酸酶抑制剂1的活性降低。β-肾上腺素能受体结合和基础和肾上腺素刺激的腺苷酸环化酶的活动减少肌肉颗粒部分甲状腺功能减退症大鼠。丙硫氧嘧啶治疗3周后，给予大鼠三碘甲状腺原氨酸3天，使改变的代谢参数恢复正常。建议甲状腺功能减退大鼠骨骼肌中糖原代谢酶的β-肾上腺素能反应性降低是由于磷蛋白磷酸酶活性增加以及β-肾上腺素能受体和腺苷酸环化酶活性降低。
The effects of hypothyroidism on glycogen metabolism in rat skeletal muscle were studied using the perfused rat hindlimb preparation. Three weeks after propylthiouracil treatment, serum thyroxine was undetectable and muscle glycogen and Glc-6-P were decreased. Basal and epinephrine-stimulated phosphorylase a and phosphorylase b kinase activities were also significantly reduced, as were epinephrine-stimulated cAMP accumulation and cAMP-dependent protein kinase activity. Conversely, basal and epinephrine-stimulated glycogen synthase I activities were significantly higher while the Ka of the enzyme for Glc-6-P was lower in hypothyroid animals. Propylthiouracil-treated rats also had increased phosphoprotein phosphatase activities towards phosphorylase and glycogen synthase and decreased activity of phosphatase inhibitor 1. beta-Adrenergic receptor binding and basal and epinephrine-stimulated adenylate cyclase activities were reduced in muscle particulate fractions from hypothyroid rats. Administration of triiodothyronine to rats for 3 days after 3 weeks of propylthiouracil treatment restored the altered metabolic parameters to normal. It is proposed that the decreased beta-adrenergic responsiveness of the enzymes of glycogen metabolism in hypothyroid rat skeletal muscle is due to increased activity of phosphoprotein phosphatases and to reduced beta-adrenergic receptors and adenylate cyclase activity.