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Are the Effects of T₃ on Resting Metabolic Rate in Euthyroid Rats Entirely Caused by T₃ Itself?

Dipartimento di Scienze Biologiche ed Ambientali (M.M., E.S., F.G.), Università degli Studi del Sannio, 82100 Benevento, Italy; Dipartimento di Scienze della Vita (A.La.), Seconda Università degli Studi di Napoli, 81100 Caserta, Italy; Dipartimento di Fisiologia Generale ed Ambientale (A.Lo., L.B.), Università di Napoli Federico II, 80134 Napoli, Italy; and Department of Radiology and Nuclear Medicine (G.P.), Benjamin Franklin Medical Center, Free University of Berlin, 12200 Berlin, Germany

Address all correspondence and requests for reprints to: Antonia Lanni, Dipartimento di Scienze della Vita, Seconda Università degli Studi di Napoli, Via Vivaldi 43, 81100 Caserta, Italy. E-mail: antonia.lanni{at}unina2.it

Because we previously reported that T₃ and 3,5-diiodo-L- thyronine (3,5-T₂) both increase resting metabolic rate (RMR), 3,5-T₂ could be another thyroidal regulator of energy metabolism. This effect of 3,5-T₂ is evident in rats made hypothyroid by propylthiouracil and iopanoic acid, not in normal euthyroid (N) rats. Possibly, under euthyroid conditions, active 3,5-T₂ may need to be formed intracellularly from a precursor such as T₃. We tested this hypothesis by giving a single injection of T₃ to N rats and comparing the time course of the variations in RMR with those of the changes in the serum and hepatic levels of 3,5-T₂. Acute injection had an evident effect on RMR, 25 h earlier, in N rats than in rats made hypothyroid by propylthiouracil and iopanoic acid, maximal values (+40%) being reached in the former at 24–26 h. In N rats, the simultaneous injection of actinomycin D with the T₃ inhibited the late part of the effect (after 24 h) more strongly than the early part (14–24 h). In serum and liver, 3,5-T₂ levels were increased significantly at 12–24 h after T₃ injection into N rats, a time at which RMR was rising rapidly to peak. These results seem to indicate that when T₃ is injected into N animals, not all the effects on RMR are attributable to T₃ itself, the early effect presumably being largely because of its in vivo deiodination to 3,5-T₂. Because the effects of T₃ and 3,5-T₂ are additive, in N rats, the two iodothyronines probably cooperate in vivo to determine the total metabolic rate.

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