Mi Z H, Tian Y, Cong Z
Department of Pharmacology, Beijing Medical University, China.
Zhongguo Yao Li Xue Bao. 1992 Jul;13(4):380-4.
The influence of hyperthyroidism on the action of drugs affecting rat liver glycogen content and its mechanism were investigated. The thyroid-induced hyperthyroidism of rat served as the model. In normal rats, dexamethasone (5 mg.kg-1, ip) increased the content of liver glycogen and decreased the Bmax of glucocorticoid receptors (GCR) in liver cytosol. These effects were minimized or even disappeared in hyperthyroid rat models. On the other hand, in normal rats, epinephrine (0.20 mg.kg-1, ip) decreased the content of liver glycogen. This effect was potentiated in hyperthyroid rat models. Epinephrine did not affect the Bmax of GCR in liver cytosol of normal and hyperthyroid rats. These results suggested that hyperthyroidism may be one of the causes effecting the individual differences of drug action, and that the influence of hyperthyroidism on the glycogen-increasing action of dexamethasone correlated well with the changes in glucocorticoid receptor. The mechanism of the influence of hyperthyroidism on the glycogen-decreasing action of epinephrine is to be further explored.
研究了甲状腺功能亢进对影响大鼠肝糖原含量的药物作用的影响及其机制。以甲状腺诱导的大鼠甲状腺功能亢进作为模型。在正常大鼠中，地塞米松（5mg·kg-1，腹腔注射）增加肝糖原含量并降低肝胞液中糖皮质激素受体（GCR）的Bmax。在甲状腺功能亢进大鼠模型中，这些作用减弱甚至消失。另一方面，在正常大鼠中，肾上腺素（0.20mg·kg-1，腹腔注射）降低肝糖原含量。在甲状腺功能亢进大鼠模型中，这种作用增强。肾上腺素对正常和甲状腺功能亢进大鼠肝胞液中GCR的Bmax无影响。这些结果表明，甲状腺功能亢进可能是影响药物作用个体差异的原因之一，且甲状腺功能亢进对地塞米松糖原增加作用的影响与糖皮质激素受体的变化密切相关。甲状腺功能亢进对肾上腺素糖原降低作用的影响机制有待进一步探讨。
