Abstract
We recently demonstrated that lowering of T3 and a rise in rT3 observed in non-thyroidal illnesses could be induced by glucagon infusion in normal subjects without altering T4. Free T4 (FT4) and T3 resin uptake (T3RU) values suggesting that altered T4 metabolism may be mainly responsible for those changes. To further assess the role of altered T4 metabolism in these changes during induction of hyperglucagonaemia, we studied glucose, T4, FT4, T3RU, T3, and rT3 concentrations before and after iv glucagon injection (0.5 mg) for up to 3 h in 6 anaesthetized dogs, since thyroxine-binding globulin (TBG) concentration is known to be extremely low in dogs. A control study was conducted with iv normal saline (0.5 ml) injection. T4, FT4 and T3RU remained unchanged during both studies. A significant fall was noted in T3 with glucagon (delta T3, 0.23 +/- 0.06 nmol/l vs 0 +/- 0.03 nmol/l with normal saline; P less than 0.01). rT3 rose markedly following glucagon infusion (delta rT3, 0.04 +/- 0.011 nmol/l vs -0.017 +/- 0.006 nmol/l with normal saline; P less than 0.01). Moreover, areas under the curves for T3 and rT3 were markedly increased during glucagon infusion when compared to saline administration (P less than 0.01 for both comparisons). Therefore, this study suggests that changes in T3 and rT3 concentrations observed in non-thyroidal illnesses may be attributed to hyperglucagonaemia and may be secondary to altered T4 metabolism as reflected by lowered T3/T4 and increased rT3/T4 ratio.
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