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Emilio Herrera, Francisco Escobar del Rey and Gabriella Morreale de Escobar


The effects of the daily feeding of 6 μg of propylthiouracil1/rat for about two weeks on the thyroid of animals maintained on different levels of iodine intake (from 0.5–3.6 μg/day/100 g BW) have been investigated. We have confirmed previous observations by other authors (Yamada & Schichijo 1962; Greer et al. 1962) showing that very low doses of PTU increase thyroid weight in rats on a low iodine supply without necessarily decreasing their rather low plasma PBI or their high thyroidal 131I uptake, and that the same doses no longer have an effect on thyroid weight if the iodine intake is raised. In the present experiments this occurred when the iodine intake was raised to about 1.2–1.3 μg/day/100 g BW. As shown here, it is unlikely that these low doses of PTU block synthesis of the thyroid hormones. They do, however, slightly inhibit the extrathyroidal deiodination of T4 and they probably trigger thyrotrophin (TSH) release from the pituitary gland. The present findings are compatible with the view that very small doses of PTU can be goitrogenic if the rats are on an iodine intake which is barely adequate for normal peripheral requirements, because these are increased chronically, even if slightly. Because of the low iodine stores the thyroid would then be unable to compensate for these increased hormone requirements. Even a small increase of available iodine may avoid this situation so that the effects of the low PTU doses are no longer detectable either in the plasma TSH activity or in the thyroid weight. The low PTU doses used here appear to hasten and aggravate a situation which would eventually develop from a more prolonged or a more severe degree of iodine deficiency only. The experimental situation induced by these low PTU doses might serve as an interesting model system for the study of simple goitre in areas in which iodine deficiency is not too extreme.

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Gabriella Morreale de Escobar, María Jesís Obregón, Carmen Ruiz de Oña and Francisco Escobar del Rey

Abstract. Thyroxine (T4) is transferred from the mother to the hypothyroid rat fetus late in gestation, mitigating T4 and T3 deficiency in fetal tissues, the brain included. We have now compared the effects of maternal infusion with T3. Normal and thyroidectomized rats were started on methimazole (MMI) on the 14th day of gestation, given alone, or together with a constant infusion of 0.45 μg (0.69 nmol) T3 or of 1.8 μg (2.3 nmol) T4/100 g per day. Maternal and fetal samples were obtained at the 21st day of gestation. The doses of T3 and T4 were biologically equivalent for the dams, as assessed from maternal plasma and tissue T3, and plasma TSH levels. MMI blocked the fetal thyroid; T4 and T3 levels were low in all fetal tissues, and fetal plasma TSH was high. Maternal infusion with T4 mitigated both T4 and T3 deficiency in all fetal tissues, the brain included, and decreased fetal plasma TSH. In contrast, infusion of T3 normalized fetal plasma T3 and increased the T3 levels in several tissues, but not in the brain. Neither did it decrease the high fetal plasma TSH levels. The results show that when the fetus is hypothyroid, T3 crosses the rat placenta at the end of gestation, but does not affect all tissues to the same degree. In contrast to the effects of maternal T4, maternal T3 does not alleviate the T3 deficiency of the brain or, presumably, of the thyrotrope. Thus, end-points of thyroid hormone action related to TSH release should not be used to measure transfer of maternal T3 to the fetal compartment. Moreover, T4 should be given, and not T3, to protect the hypothyroid fetal brain.

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Javier Sánchez-Vega, Francisco Escobar del Rey, Humberto Fariñas-Seijas and Gabriella Morreale de Escobar


To evaluate the iodine nutrition of the pregnant women of the Spanish Autonomous Community Extremadura. There are ∼10 000 births per year in Extremadura, which historically contains areas with endemic goiter (Las Hurdes).


Population study in which a representative sample of pregnant women of the general population was analyzed, along with another sample of pregnant women from traditionally goitrogenic areas. With the collaboration of selected health centers, an additional sample of blood and urine was obtained within the primary health care pregnancy-monitoring program; these samples were sent to a single central laboratory.


Biochemistry: determination of iodine and creatinine in urine, and serum concentrations of thyroxine, free thyroxine, tri-iodothyronine, TSH, thyroglobulin, and two anti-thyroid antibodies. Each parameter was measured by means of a single specific RIA.


Changes between the first trimester and later stages of pregnancy of all biochemical variables studied corresponded with those described for other European areas with a comparable iodine nutrition. Using the urinary iodine concentration value as an indicator of iodine ingestion, it was found that in the first trimester of pregnancy six out of ten women from Extremadura ingested less than the currently recommended amount (250 μg I/day), and approximately three out of ten of these women ingested less than half of this amount.


It is imperative to implement in all Extremadura the generalized and controlled use of complements that contain 200–250 μg I/day throughout pregnancy and, if possible, before.

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Francisco Escobar del Rey, Carmen Ruiz de Oña, Juan Bernal, Maria Jesus Obregón and Gabriella Morreale de Escobar

Abstract. Rats fed a low iodine diet have decreased total and nuclear T3 concentrations in the liver and brain, as compared with rats supplemented with iodine, possibly because of the very low plasma and tissue T4 pools in low-iodine diet rats, leading to decreased intracellular generation of T3 in those tissues. If so, T3 levels should not decrease in heart and skeletal muscle, as plasma T3 is normal in low-iodine diet rats and these two tissues derive their intracellular T3 directly from plasma T3. We have studied this point in male rats fed a low-iodine diet, a low-iodine diet + iodine, and the stock diet. As in previous studies, low-iodine rats had very low plasma T4 and high plasma TSH levels, plasma T3 levels being normal. Liver T3 decreased, and so did the brain T3 levels despite a compensatory increase in type II 5' iodothyronine deiodinase activity. Contrary to expectations, T3 concentrations were lower in the heart and skeletal muscle of low-iodine diet rats. Attempts to clarify the possible mechanism(s) involved have been unsuccessful so far. The present results show that, despite normal plasma T3, a deficiency of T3 occurs in more tissues of rats on a low iodine intake than previously assumed. If the present results are pertinent to inhabitants from areas with severe iodine dificiency, it would appear that they might suffer from a generalized tissue T3 deficiency (and hypothyroidism?), even if overt clinical signs are not usually present.