MECHANISM OF THYROID-INDUCED CREATINURIA IN RAT, WITH SPECIAL REFERENCE TO CREATINE SYNTHESIS IN LIVER AND CREATINE LOSS FROM SKELETAL MUSCLE

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Abstract
The mechanism of thyroid-induced creatinuria was investigated in rats. Rats were injected with triiodothyronine (T3) (100 .mu.g/100 g, s.c.) at 9.00 h. O2 consumption increased 12 h after T3 injection, reaching a peak value 48 h after the injection and decreasing to the pre-injection level at 96 h. Urinary creatine excretion increased during the 1st 10 h after the injection, approaching a maximal value 34-48 h after the injection and decreasing to the pre-injection level 72-82 h after the injection. Throughout the experimental period, urinary creatinine decreased with time after the injection, although the difference between the groups was not significant. A decreased creatine tolerance was observed after T3 injection. .beta.-Guanidinopropionic acid (.beta.-GPA), a competitive inhibitor of creatine transport into skeletal muscle, and partial hepatectomy, which inhibits creatine synthesis, were without effect on the difference in urinary creatine excretion between T3-treated and control animals. T3 increased the plasma creatine level both in bilateral nephrectomized and in bilateral nephrectomized plus .beta.-GPA administrated groups. Increased creatine loss from skeletal muscle in addition to decreased creatine uptake of skeletal muscle, rather than increased hepatic synthesis of creatine, probably play an important role in T3-induced creatinuria.