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Mechanism of thyroid-induced creatinuria was investigated in rats. The rats were injected with triiodothyronine (T3) (100 mug/100g, sc) at 9.00 hr. Oxygen consumption increased 12 hr after T3 injection, reaching peak value 48 hr after the injection and decreasing to the pre-injection level at 96 hr. Urinary creatine excretion also increased during the first 10 hr after the injection, approaching maximal value 34-48 hr after the injection, and decreasing to the pre-injection level 72-82 hr 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 also observed after T3 injection. Beta-Guanidinopropionic acid (beta-GPA), a competitive inhibitor of creatine transport into skeletal muscle, as well as partial hepatectomy, caasing inhibition of 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. These results suggest that increased creatine loss from skeletal muscle in addition to decreased creatine uptake of skeletal muscle rather than increased hepatic synthesis of creatine play an important role in T3-induced creatinuria.

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