Abstract
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 (T3) 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 T3 and thyroxine levels than controls at 110 f and showed a higher postnatal surge in T3. Maximal T3 binding capacity (Bmax, pmol T3/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, Bmax 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; Bmax values were reduced in liver but increased in muscle. Postnatally, lower muscle Bmax values occurred in parallel with transient higher levels of circulating T3. 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.(ABSTRACT TRUNCATED AT 250 WORDS)
Published Version
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