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大鼠中三碘甲状腺原氨酸诱导肌酸尿的机制。

Mechanism of triiodothyronine-induced creatinuria in the rat.

作者信息

Kurahashi M, Kuroshima A

出版信息

Am J Physiol. 1977 Aug;233(2):E91-6. doi: 10.1152/ajpendo.1977.233.2.E91.

Abstract

Mechanism of triiodothyronine (T3)-induced creatinuria was studied in rats after a single injection of T3 (100 microgram/100 g per s). Urinary creatine excretion increased markedly during the 1st day after T3 injection. Peak of creatinuria was observed during the 2nd day after T3 injection. Excretions of nonprotein nitrogen and potassium were not different between control and T3-injected animals throughout the experimental period. Creatine reabsorption in the kidney was not influenced by T3 treatment. Radioactive creatines in both plasma and urine after [14C]creatine injection were higher in T3-injected animals than in controls, whereas the uptake of radioactive creatine by muscle was lower in the former. Creatine content in muscles decreased significantly 48 h after T3 injection. Moreover, T3 increased a fraction derived from muscle in urinary creatine, but it did not influence that derived from creatine synthesized de novo. These results suggest that both decreased creatine uptake by muscle and increased release of creatine from muscle play important roles in T3-induced creatinuria.

摘要

研究了大鼠单次注射三碘甲状腺原氨酸(T3,100微克/100克体重)后T3诱导肌酸尿的机制。T3注射后第1天尿肌酸排泄显著增加。在T3注射后第2天观察到肌酸尿峰值。在整个实验期间,对照动物和注射T3的动物的非蛋白氮和钾排泄没有差异。T3处理不影响肾脏对肌酸的重吸收。注射[14C]肌酸后,注射T3的动物血浆和尿液中的放射性肌酸高于对照动物,而前者肌肉对放射性肌酸的摄取较低。T3注射48小时后肌肉中的肌酸含量显著降低。此外,T3增加了尿肌酸中来自肌肉的部分,但不影响从头合成的肌酸衍生部分。这些结果表明,肌肉对肌酸摄取的减少和肌肉中肌酸释放的增加在T3诱导的肌酸尿中起重要作用。

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