PERINATAL ONTOGENY OF PORCINE NUCLEAR THYROID-HORMONE RECEPTORS AND ITS MODULATION BY THYROID STATUS

Induction of nuclear thyroid hormone receptors (TRs) represents a key point in the control of growth, development, differentiation, and metabolism of most tissues. The influence of thyroid status on the ontogeny of hepatic and skeletal muscle TRs has been investigated in perinatal pigs. Plasma concentrations of total and free 3,5,3'-triiodothyronine (T-3) increased markedly from 80 days of fetal life (80 f) to 2 days of postnatal life. Test piglets obtained from sows fed a high glucosinolate rapeseed diet had lower T-3 and thyroxine levels than controls at 110 f and showed a higher postnatal surge in T-3 Maximal T-3 binding capacity (B-max, pmol T-3/mg DNA, means +/- SE) in liver increased from 0.07 +/- 0.01 at 80 f to 0.37 +/- 0.02 at birth and then plateaued. In longissimus dorsi muscle, B-max values were much higher than in liver and increased from 0.90 +/- 0.02 at 80 f to 1.37 +/- 0.13 at birth and then declined to 1.09 +/- 0.11 at 2 days of age. Long-term fetal hypothyroidism affected the ontogenic profile of both liver and muscle receptors but in opposite directions; B-max values were reduced in liver but increased in muscle. Postnatally, lower muscle B-max values occurred in parallel with transient higher levels of circulating T-3. Apparent binding affinities were slightly different in liver and muscle during fetal life, and there was an effect of age in muscle. In conclusion, as far as the receptor is concerned, fetal muscle can potentially respond to thyroid hormones much earlier in development than the liver. It is suggested that thyroid hormones could play a role in modulating the expression of their receptors during fetal life, although other factors may be more important in the perinatal period because of T-3-independent changes in the receptors. Finally, a differential expression of the isoforms of TR within tissues is suggested during fetal life.