"Differential and tissue-specific modulation of T3 and 9-cis retinoid acid receptors by IGF-1 in the rat"

PELLIZAS, CG; MONTESINOS, MM; MASINI-REPISO AM; TORRES AI; COLEONI AH

MARY ANN LIEBERT INC

Lugar: New York; Año: 2002 vol. 12 p. 1071 - 1071

riiodothyronine (T3) exerts most of its effects through nuclear thyroid hormone receptors (TRs) that  bind mainly as heterodimers with retinoid-X receptors (RXRs) to thyroid hormone response  elements in target genes. It is well known that T3 activates the growth hormone (GH)-insulin-like    growth factor I (IGF-I) axis in rats. In turn, IGF-I inhibits the T3-induced GH production in cell  cultures. The impact of IGF-I on T3 action has only been partially explored. We have presented evidence that IGF-I feeds back to limit specific metabolic actions of T3 in rat liver through a downregulation of nuclear TR number and its mRNA expression. We have also found that IGF-I injected to rats inhibited pituitary GH production. In this study we aimed at exploring whether the IGF-I-induced feedback loop on T3-action in the liver also operates in the pituitary gland. The mechanism of the liver TR mRNA reduction induced by IGF-I was also studied. We evaluated the effect of recombinant human (rh) IG