Endocytosis of Thyroglobulin and Release of Thyroid Hormone in Mice by Catecholamines and 5-Hydroxytryptamine

Ericson, Lars; Melander, Arne; Owman, Ch.; Sundler, F.

doi:10.1210/endo-87-5-915

Cited by 45 publications

(12 citation statements)

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“…Serotonin, by its paracrine action on the follicular cells, could stimulate the endocytosis of thyroglobulin and the release of T, and T,. Thus secretory products of parafollicular cells could act as intrathyroid local hormones, as has been suggested for mice by Ericson et al (1970), and in vitro for sheep and bats by Gershon (1982, 1983). Gershon et al (19781 showed in the in vitro experiments on bat and mice thyroid lobes, that serotonin was released from parafollicular cells by elevating the external calcium-ion concentration; serotonin release was accompanied by ultrastructural signs of activation of the follicular cells.…”

Section: Discussionmentioning

confidence: 76%

The effect of chronic hypercalcemia or hypocalcemia on the follicular and parafollicular cells in rat thyroid gland

et al. 1990

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In three experiments of 30 weeks' duration, 93 adult female Wistar rats received controlled amounts of calcium with food and water, to produce a state of either hypercalcemia or hypocalcemia. A systematic stereological analysis of the thyroid glands and a radioimmunological analysis of thyroxine, triiodothyronine, and thyrotropine were performed. In the hypercalcemic rats, a reactive hyperplasia of the parafollicular cells was established; this was accompanied by morphological and biochemical signs of hyperfunction of the follicular cells, despite a reduced central stimulation by thyrotropin. In the hypocalcemic animals, no quantitative morphological changes in the parafollicular cells were observed; however, morphological and biochemical signs of hypofunction of the follicular cells were obvious, despite stronger central stimulation by thyrotropin. It is concluded that the extrinsic regulation of follicular cells by the blood calcium level is stronger than the intrinsic regulation by hypothalamo-hypophyseal hormones.

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Section: Discussionmentioning

confidence: 76%

The effect of chronic hypercalcemia or hypocalcemia on the follicular and parafollicular cells in rat thyroid gland

et al. 1990

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“…Thus, quite possibly the increased level of plasma 5-HT could be due to either increased synthesis or decreased degradation or both. As 5-HT may stimu¬ late thyroid hormone secretion as well as thyroid blood (1,3,12), it is possible that the increased level of plasma 5-HT in hyperthyroidism augments the hypersecretion of thyroid hormone. The increased circulating level of histamine in hyper¬ thyroid patients may possibly be due to decreased activity of histaminase, a degrading enzyme for hista¬ mine.…”

Section: Discussionmentioning

confidence: 99%

“…It has been reported that 5-hydroxy¬ tryptamine ( 5-HT) activity stimulates iodine metabolism in isolated thyroid cells which leads to the formation of iodothyronines, this effect being similar to that of catecholamines (2). Ericson et al (3) showed that both 5-HT and catecholamines stimulate thyroid hormone release in vivo. Further, 5-hydroxytryptophane is known to elevate TSH secretion in rats and humans (4,5), and it has been reported that intravenous injection of histamine H?…”

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confidence: 99%

Biogenic amines and thyrotoxicosis

Upadhyaya

Agrawal²,

Gp³

et al. 1992

Acta Endocrinologica

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Circulating levels of T3, T4, \g=g\-amino-butyricacid, glutamate, 5-hydroxytryptamine, histamine, monoamine oxidase and histaminase were studied in 45 (2 5M, 20F) hyperthyroid patients and 46 (2 5M, 21F) normal healthy volunteers. Increased levels of blood 5-hydroxytryptamine, histamine and glutamic acid were observed along with elevated T3 and T4, whereas plasma \g=g\-aminobutyric acid, monoamine oxidase and histaminase activities were found to be low in both male and female patients.After three months of treatment, circulating levels of 5-hydroxytryptamine, histamine and glutamic acid decreased significantly along with normalization of thyroid hormones and with an increase in the concentrations of \g=g\-aminobutyric acid, monoamine oxidase and histaminase. There was a positive correlation between these amines and thyroid hormone levels. The findings thus suggest that alterations in the metabolism of biogenic amines may be related to an altered metabolism in thyrotoxicosis, and these parameters may prove to be useful markers for diagnosis and follow-up of these patients.Biogenic amines play an important role in the regulation of many physiological and psychological processes. Recently, considerable attention has been paid to eva¬ luating the effect of biogenic amines on thyroid function. It has been observed that not only TSH but also longacting thyroid stimulator (LATS) may interact with biogenic amines (1). Experimental studies have also shown a close association between biogenic amines and thyroid function. It has been reported that 5-hydroxy¬ tryptamine ( 5-HT) activity stimulates iodine metabolism in isolated thyroid cells which leads to the formation of iodothyronines, this effect being similar to that of catecholamines (2). Ericson et al.(3) showed that both 5-HT and catecholamines stimulate thyroid hormone release in vivo. Further, 5-hydroxytryptophane is known to elevate TSH secretion in rats and humans (4, 5), and it has been reported that intravenous injection of histamine H? agonist enhances Tj response to TRH and thus interacts with thyroid function. Sanchez Herrenz et al. (6) on the other hand reported that y-aminobutyric acid (GABA) inhibits TSH release in experimental ani¬ mals. Thus, it was considered to be of interest to study the metabolic status of these amines in hyperthyroid patients in order to elucidate the possible association of these amines with thyroid dysfunction.Patients and methods We studied 46 (2 5M, 2 IF) normal healthy volunteers (as controls), aged 25 to 45 years, non-obese, with normal endocrine and metabolic functions, and with no family history of thyrotoxicosis; and 45 (25M, 20F) hyperthyroid patients, aged 20 to 50 years. The diagno¬ sis of thyrotoxicosis was based on clinical profile and biochemical investigations including measurements of serum T? and T4 (RIA methods). All the subjects were selected from the Thyroid Clinic of S.S. Hospital, Institute of Medical Sciences, Bañaras Hindu University. None of the controls were taking any drug or intoxicants like alcohol, mar...

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“…Modifications of plasma TSH in primary hypothyroidism may be due to an action of L-dopa through its metabolites dopamine and norepinephrine, at the hypothalamic or pituitary level, or indirectly through an effect at the thyroid level. Because no modifications of plasma total-T* and its functional turnover are present in primary hypo thyroidism after L-dopa [Rapoport et al, 1973], a delayed inhibition of TSH due to a release of thyroid hormones by dopamine, as is the case in normal subjects [Ericson et a l, 1970;Melander and Sundler, 1972], can be ex cluded. On the contrary, an effect of L-dopa and/or its metabolites directly at the pituitary level must be considered when taking into account that chronic treatment with L-dopa succeeds in inhibiting the TSH response to TRH [Spaulding et al, 1972], Finally, another possible action site of the catecholamine precursors could be the hypophysiotropic area of the hypothalamus.…”

Section: Discussionmentioning

confidence: 99%

Effect of L-Dopa on Plasma TSH Levels in Primary Hypothyroidism

Minozzi¹,

Faggiano²,

Lombardi³

et al. 1975

Neuroendocrinology

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Plasma TSH responses after an i.v. injection of 100 mg of L-dopa were evaluated by radioimmunoassay in 4 normal euthyroid subjects and in 8 patients with primary hypothyroidism. In agreement with previous results, no variations in plasma TSH levels were observed in the euthyroid subjects. In contrast, in primary hypothyroidism L-dopa induced a biphasic response in plasma TSH. In fact, we observed a transitory increase with a maximum at 30 min (mean ± SEM = 54 ± 18%) followed by a decrease reaching a minimum level of plasma TSH basal values at 90 min (mean ± SEM = 15 ± 6%). These findings demonstrate that the plasma TSH response to L-dopa in primary hypothyroidism is time-dependent. Some speculation on the possible mechanism of this action is presented.

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Endocytosis of Thyroglobulin and Release of Thyroid Hormone in Mice by Catecholamines and 5-Hydroxytryptamine

Cited by 45 publications

References 0 publications

The effect of chronic hypercalcemia or hypocalcemia on the follicular and parafollicular cells in rat thyroid gland

The effect of chronic hypercalcemia or hypocalcemia on the follicular and parafollicular cells in rat thyroid gland

Biogenic amines and thyrotoxicosis

Effect of L-Dopa on Plasma TSH Levels in Primary Hypothyroidism

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