Regulation of porcine skeletal muscle nuclear 3,5,3′-tri-iodothyronine receptor binding capacity by thyroid hormones: modification by energy balance

Author:

Morovat A,Dauncey M J

Abstract

Abstract Thyroid hormones have been implicated in the regulation of nuclear 3,5,3′-tri-iodothyronine (T3) receptor binding capacity (Bmax) but, despite numerous in vivo and in vitro studies, there is considerable controversy regarding their exact role. Since changes in thyroid status alter energy balance and hence may influence T3 receptor numbers, the effects of chronic hypothyroidism and T4 treatment have been studied in young pigs under conditions of controlled energy intake. Four groups of animals comprising a hypothyroid, a euthyroid and a hyperthyroid group, all on the same level of food intake, and a hyperthyroid group on twice the amount of food were used. After 3 weeks on the treatment regimes, both the hypothyroid animals on the same level of food intake and the hyperthyroid animals on twice the amount of food had significandy increased Bmax values (97% and 137% higher respectively) compared with euthyroid controls. However, there was no difference between controls and the hyperthyroid animals on the same level of food intake. In a second study, the effects of short-term treatment of euthyroid animals with T3 was investigated. Results showed that in two groups of controls that received intravenous saline, those on a higher food intake had higher Bmax values (76% increase). Intravenous T3 administration to animals on a low food intake did not change the receptor numbers. In none of the studies was there any change in the dissociation constant of the receptors as a result of different treatments. It is suggested that, at least in postnatal life, thyroid hormones per se have no significant effect on nuclear T3 receptor numbers in skeletal muscle. Instead, changes in Bmax in response to thyroid status may be secondary to alterations in energy balance induced by these hormones. Journal of Endocrinology (1995) 144, 233–242

Publisher

Bioscientifica

Subject

Endocrinology,Endocrinology, Diabetes and Metabolism

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