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F. Escobar del Rey and G. Morreale de Escobar

Among the different factors which may influence the peripheral needs for thyroid hormone, changes in environmental temperature seem to have been most extensively studied. Different workers in this field (Bondy et al., 1952, Leblond et al., 1952, Rand et al., 1952, Kassenaar et al., 1956) were able to show by different types of experiments, that prolonged exposure to low temperatures is accompanied by an increase in peripheral thyroxine requirement. Kassenaar et al. (1956) clearly showed that these experiments have preferably to be done on thyroidectomized, thyroxine maintained animals as compensatory action may mask the results when intact animals are used.

Contrary to this, very little is known about the influence of muscular exercise on the thyroxine disappearance rate: Bondy & Hagewood (1952) not only studied the effect of low temperatures, starvation and cortisone on the PBI

1. The first paper, on »The effect of environmental temperature on the blood protein

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F. Escobar del Rey and G. Morreale de Escobar

No conclusive evidence on the influence of muscular exercise on thyroxine disappearance rate has yet been obtained. Bondy & Hagewood (1952) found a significant decrease in the PBI of rats after swimming for two hours. They used intact and thyroidectomized, thyroxine maintained rats, the latter being used in order to avoid a compensatory action of the thyroid. Lashof, Bondy & Sterling (1954) were, however, unable to observe any difference in the PBI and in the slope of the I131 labeled 1-thyroxine disappearance curve of healthy subjects after walking for 14 miles or swimming at full speed for 15 minutes. The thyroid function in these subjects had been previously blocked with iodide. The authors also state that muscular exercise does not increase the peripheral needs for thyroid hormone and that the differences in the PBI of swimming and control rats found in their first experiment (Bondy & Hagewood, 1952) were

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F. Escobar del Rey and G. Morreale de Escobar

Continuing previous studies on the possible effect which hypermetabolism producing factors may have on the peripheral degradation of 1-thyroxine in the rat (Kassenaar et al., 1956, Escobar del Rey & Morreale de Castro, 1956 a, 1956 b), it appeared of interest to investigate the action of 2,4 dinitrophenol (DNP), which is known to produce hypermetabolism in several animal species (Thomson et al., 1935).

The well known finding of a lowering of the serum PBI following the administration of DNP was first reported for the rat by Wolf et al. (1950) and for man by Castor & Beierwaltes (1955). The concomitant finding of a sharply lowered serum PBI and an apparently unaltered thyroid function (Wolff et al., 1950) seemed to indicate a lack of response of the hypophysis to the low levels of circulating hormone, which was later confirmed histologically by Goldberg & Chaikoff (1951). The very extensive work carried out

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F. Escobar del Rey and G. Morreale de Escobar

ABSTRACT

The effect of BHDB is determined on: a) the rate and mode of disappearance of [131I] l-thyroxine in thyroidectomized, l-thyroxine maintained rats, and b) the concentration of iodine-containing compounds in the body and excreta of thyroidectomized rats, isotopically equilibrated with l-thyroxine or l-triiodothyronine. Labelled thyroxine is rapidly excreted into the intestines and faeces of BHDB-treated rats and this alteration precedes a much less marked decrease of the urinary radioiodide. In isotopically equilibrated rats it is shown that during the first few days of BHDB administration there is a decrease of the urinary iodide, which later reverts to normal or, in the case of triiodothyronine maintained rats, increases well above normal values. The alterations of urinary iodide excretion are more than accounted for by opposite changes in the faecal excretion of iodinated compounds. BHDB results in a depletion of the hormonal pool in the peripheral tissues of thyroxine-maintained rats, but this is not so in the case of triiodothyronine-maintained animals. It is concluded that there is more evidence in favour of the interpretation that BHDB alters the availability of the thyroid hormone to peripheral tissues than in favour of an inhibition of peripheral deiodinating systems. It is suggested that the marked loss of thyroxine from the body of BHDB-treated rats might be the underlying cause of its »antithyroxine« action.

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F. Escobar del Rey and G. Morreale de Escobar

Conclusive evidence on the effect of 2,4 dinitrophenol (DNP) on the rate of breakdown of thyroid hormone(s) is not available.

The plasma I131 labeled 1-thyroxine disappearance curves obtained by Goldberg and associates (1955) in intact, propylthiouracil treated rats under the influence of DNP, and the observation made by Castor & Beierwaltes (1956) that the serum PBI of an athyreotic, thyroid maintained patient, decreased after the administration of DNP, strongly suggest that peripheral factors influenced the level of circulating thyroid hormone(s). The influence of DNP on the I131 distribution pattern in thyroidectomized, 1-thyroxine maintained rats. 24 hours after the injection of I131 labeled 1-thyroxine was studied in an attempt to obtain sufficient information to allow definitive conclusions (Escobar del Rey & Morreale de Escobar, 1958 a).

It was found that, though the radioactivity of the serum was definitely lower in the DNP treated animals and this decrease was

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G Morreale de Escobar, MJ Obregon and F Escobar del Rey

The present comments are restricted to the role of maternal thyroid hormone on early brain development, and are based mostly on information presently available for the human fetal brain. It emphasizes that maternal hypothyroxinemia - defined as thyroxine (T4) concentrations that are low for the stage of pregnancy - is potentially damaging for neurodevelopment of the fetus throughout pregnancy, but especially so before midgestation, as the mother is then the only source of T4 for the developing brain.Despite a highly efficient uterine-placental 'barrier' to their transfer, very small amounts of T4 and triiodothyronine (T3) of maternal origin are present in the fetal compartment by 4 weeks after conception, with T4 increasing steadily thereafter. A major proportion of T4 in fetal fluids is not protein-bound: the 'free' T4 (FT4) available to fetal tissues is determined by the maternal serum T4, and reaches concentrations known to be of biological significance in adults. Despite very low T3 and 'free' T3 (FT3) in fetal fluids, the T3 generated locally from T4 in the cerebral cortex reaches adult concentrations by midgestation, and is partly bound to its nuclear receptor. Experimental results in the rat strongly support the conclusion that thyroid hormone is already required for normal corticogenesis very early in pregnancy.The first trimester surge of maternal FT4 is proposed as a biologically relevant event controlled by the conceptus to ensure its developing cerebral cortex is provided with the necessary amounts of substrate for the local generation of adequate amounts of T3 for binding to its nuclear receptor. Women unable to increase their production of T4 early in pregnancy would constitute a population at risk for neurological disabilities in their children. As mild-moderate iodine deficiency is still the most widespread cause of maternal hypothyroxinemia in Western societies, the birth of many children with learning disabilities may already be preventable by advising women to take iodine supplements as soon as pregnancy starts, or earlier if possible.

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A. Aranda, F. Hervás, G. Morreale de Escobar and F. Escobar del Rey

ABSTRACT

Pituitary LH was studied by means of a specific radioimmunoassay (RIA) in male rats at different time intervals after thyroidectomy (T̄), and in rats which were T̄ at least 30 days before and were then treated with different doses of L-thyroxine or triiodo-L-thyronine.

A decrease in the pituitary LH of the T̄ animals, with respect to the intact age-paired controls, was demonstrable from 13 days after the operation, when total pituitary LH content was taken into consideration, or from 5 days after T̄, when the LH concentration (μg/mg pituitary) was considered. Doses of thyroid hormones lower than the daily maintenance dose for the rat produced very little effect on the pituitary LH levels of T̄ animals. However, a single dose of 1.75 μg of T4 or 0.2 μg of T3 (doses approximately equivalent to the T4 and T3 maintenance dose for T̄ rats) induced such a rapid and intense increase in the pituitary LH content that it no longer differed from that of the intact age-paired controls by 12 hours. Surprisingly, 5.0 μg of T4 and 1.0 μg of T3 did not produce any increase in the pituitary LH content of T̄ rats.

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F. Escobar del Rey, G. Morreale de Escobar, M. D. Garcia Garcia and J. Mouriz Garcia

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G. Morreale de Escobar, F. Escobar del Rey and P. Llorente Rodríguez

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H. Studer, H. Bürgi, H. Kohler, M. C. García and G. Morreale de Escobar

ABSTRACT

Small doses of iodide (2 times 3.2 μg at 12 h interval), below those capable of inducing Wolff-Chaikoff effect, were injected into rats kept on a moderately low iodine diet. By means of a 125I equilibration technique as well as by direct measurement of cold T4, it was demonstrated that the level of circulating PB125I (representing iodothyronines as confirmed by column chromatography) increased by a mean of 40% within 24 h following the first iodide injection. The serum TSH concentration (measured by radioimmunoassay) was simultaneously depressed.

Thus, in stimulated thyroid glands, a biologically significant fraction of an iodide load escapes autoregulatory control of iodothyronine synthesis. A small, transient increase of hormone release is likely to represent the physiological response of a normal gland to a sudden supplement of iodide supply. The ensuing depression of TSH secretion may be necessary for final adjustment of thyroid function. It is considered to be the last step in a cascade of mechanisms whose interaction keeps the thyroidal hormone output within narrow limits in the face of a fluctuating iodide supply. Failure of one or several of these mechanisms in the goitrous human gland could conceivable explain the phenomenon of "Jod Basedow".