Differential Modulation of Liver and Pituitary Triiodothyronine and 9-cis Retinoid Acid Receptors by Insulin-Like Growth Factor I in Rats

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

THYROID

Mary Ann Liebert, Inc

Lugar: New York, U.S.A; Año: 2002 vol. 12 p. 1071 - 1071

1050-7256

font size="2"> Triiodothyronine (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