Triiodothyronine metabolism in diabetic rats.

Abstract

ABSTRACT Triiodothyronine (T3) metabolism was assessed in untreated and in insulin-treated diabetic rats and the results compared with a corresponding control group. Male rats of the Wistar strain were made diabetic by the intraperitoneal injection of alloxan in a dose of 17.5 mg/100 g body weight and thereafter maintained normoglycaemic for a week and until 24 h before initiation of the study. The average glycaemia in control and in insulin-treated animals was 135 mg/100 ml, whereas in the untreated diabetic rats it was 455 mg/100 ml. Each animal was injected a tracer dose of [125I]T3 containing 2 μCi of 125I and 15 ng of T3. Heparinized blood samples were obtained by cardiac puncture at 5, 18 and 24 h following the injection of the tracer. The excretion of inorganic 125I in the 24-h collections of urine was also determined. The kinetics of [125I]T3 were studied by the extrapolation method using the straight line of plasma disappearance between 5 and 24 h. It was found that the untreated diabetic rats had a significant slowing of plasma disappearance of labelled T3. The decrease in fractional hormone turnover was balanced by a slight expansion of the distribution space, which presumably led to a larger hormone pool and a normal degradation rate of T3. These events seemed substantiated by the normal excretion of 125I in the urine observed in untreated animals. A parallel study of plasma hormone binding using a red cell uptake method showed a significant reduction of binding avidity for T3 by plasma proteins in the untreated diabetic animals. The administration of insulin restored plasma T3 kinetics and binding avidity to normal, as observed in control rats. It was concluded that untreated diabetes mellitus induced changes in T3 kinetics and in T3 serum binding without altering hormone deiodination, parameter which reflects tissue utilization of T3.