Feto-Maternal thyroidal relationships in iodine deficiency: an experimental approach

Abstract

The multiple mechanisms which permit compensatory adaptation of the thyroid gland to severe and chronic iodine deficiency (ID) are known since many years. As a result there is a shift in the synthesis of T4 in favour of T3 and a preferential secretion of T3 over T4, so that with very little iodine normal circulating T3 is maintained despite very low T4. Overt clinical hypothyroidism is not apparent and is attributed to the normal serum T3. Here we will summarize information regarding extrathyroidal responses to ID in the rat, with special attention to the fetus and newborn and its brain during early development, as studied in our laboratory.