Inhibition of thyroid-stimulating hormone stimulation of protein kinase, glucose oxidation, and phospholipid synthesis in thyroid slices previously exposed to the hormone.

Field, James B.; Bloom, Gail; C, Chou; Kerins, Mary E.

doi:10.1172/jci108684

Cited by 39 publications

(3 citation statements)

References 21 publications

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“…In addition, the previous data indicated that refracto riness of thyroid cells to TSH stimulation could be ascribed basically to the change in the protein kinase and phospholi pid synthesis [12], rather than TSH receptors in the thyroid cells [12,30]. Eventually, the depleted amount of pituitary TSH may be responsible for TSH refractoriness to TRH [15], These observations have yielded the present data to the possibility that postreceptor events in the anterior pituitary may contribute to a predominant induction by TRH of re fractoriness of TSH secretion.…”

Section: Discussionmentioning

confidence: 98%

Role of the Hypothalamic TRH in the Regulation of Its Own Receptors in Rat Anterior Pituitaries

Mori¹,

Yamada²,

Kobayashi³

1988

Neuroendocrinology

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We explored whether endogenous TRH in the hypothalamus produced a potential change in its receptors in the rat anterior pituitary. Thyroidectomy caused a progressive increase in the pituitary TRH binding with a concomitant increase in the blood TSH level. Injection of T₄prevented the increase in the pituitary TRH binding and the blood TSH level after thyroidectomy. The hypothalamic deafferentation and electrolytic lesions in the hypothalamic paraventricular nuclei led to a significant reduction in both the content of TRH in the hypothalamic median eminence and the blood TSH level, but they affected neither the number nor affinity constant of the pituitary TRH receptors in thyroidectomized rats. The present data provide evidence that TRH receptors in the anterior pituitary are profoundly regulated by thyroid hormones, but not significantly by TRH in the hypothalamus in the rat.

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Section: Discussionmentioning

confidence: 98%

Role of the Hypothalamic TRH in the Regulation of Its Own Receptors in Rat Anterior Pituitaries

Mori¹,

Yamada²,

Kobayashi³

1988

Neuroendocrinology

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“…The mechanism of TSH-induced desensitiza¬ tion is not completely understood, but it is associ¬ ated with decreased adenylate cyclase response to TSH stimulation in thyroid plasma membrane (Shuman et al 1976;Rapoport & Adams 1976), no change in the binding of TSH to the mem¬ brane (Rapoport & Adams 1976;Field et al 1977;Totsuka et al 1983), the catalytic component of the enzyme (Shuman et al 1976;Totsuka et al 1983), cyclic nucleotide phosphodiesterase activity (Shuman et al 1976;Rapoport & Adams 1976), and the efflux of cAMP from the thyroid cells (Filetti et al 1981). Therefore, these seems to be an uncoupling of the adenylate cyclase catalytic unit from the TSH receptor.…”

Section: Discussionmentioning

confidence: 99%

Lack of desensitization of 3',5'-cyclic AMP response to thyrotropin stimulation in differentiated thyroid carcinoma

Hamada

Manabe²,

Saito³

et al. 1987

Acta Endocrinologica

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The course of the cAMP response to thyrotropin (TSH) in 23 specimens of differentiated thyroid carcinoma and the adjacent normal tissue was studied.In the carcinomatous tissue, the cAMP concentration in slices incubated with TSH was significantly greater after 2 h than after 15 min of incubation; the level was almost the same at both times in normal tissue. The effects of an initial exposure of thyroid slices to TSH (50 U/l on the subsequent cAMP responsiveness to the hormone were investigated in seven more differentiated thyroid carcinomas. In normal tissue, the cAMP level in slices exposed to TSH, washed, and exposed again was lower after the third incubation than in slices exposed to TSH only in the third. In contrast, the cAMP level tended to be greater after the second of 2 TSH incubations in 5 out of the 7 specimens of carcinomatous tissue. The data suggest that differentiated thyroid carcinoma lacks desensitization of the cAMP response to TSH.

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“…Field et al (1977) demonstrated refractori¬ ness to TSH of thyroid protein kinase, glucose oxidation and phospholipid synthesis. Rapoport 8c Adams (1976) showed refractoriness to TSH of thyroid cAMP response in cultured thyroid cells.…”

Section: Hitoshi Ikeda and Shigenobu Nagataki1mentioning

confidence: 99%

Lack of refractoriness to stimulation with long acting thyroid stimulator of thyroid hormone synthesis and thyroid hormone secretion in mice in vivo

Ikeda¹,

Nagataki

1983

Acta Endocrinologica

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The present study was undertaken to examine whether long acting thyroid stimulator (LATS) induces refractoriness of thyroid hormone synthesis and thyroid hormone secretion to the stimulator in vivo. Male DDY mice fed with a low iodine diet and given 5 \g=m\g/ml of triiodothyronine (T3) in drinking water ad libitum for 4 days were injected with 0.25 ml of LATS positive serum (1000%/0.25 ml in the McKenzie bioassay) ip every 24 h for 9 days. Groups of 5 mice were sacrificed before and 1, 3, 5, 7 and 9 days after the first injection of LATS for the determinations of serum thyroxine (T4) concentrations, the 1 h thyroid 131I uptake and thyroid weight. Control mice were injected with LATS negative pooled normal sera. Serum T4 concentrations elevated significantly 24 h after the 3rd injection of LATS and remained elevated until the end of the experiment. One hour thyroid 131I uptake elevated about 3-fold 24 h after the first injection of LATS. It further increased 24 h after the 3rd injection of LATS to 10-fold of the value for control animals and stayed elevated at this same level for the remainder of the study.These results indicate that stimulating effects of LATS on thyroid hormone synthesis assessed by thyroid 131I uptake and thyroid hormone secretion assessed by serum T4 concentrations were not diminished by the prior administration of the stimulator. These findings suggest that LATS does not induce refractoriness of either thyroid hormone synthesis or thyroid hormone secretion to the stimulator in mice in vivo. Since 1976 when Shuman et al. (1976) demonstra¬ted that the exposure of thyroid slices to thyroid stimulating hormone (TSH) induces refractoriness of the cyclic AMP system to subsequent hormone stimulation in vitro, many studies have been done with regard to refractoriness to TSH in thyroid tissue. Field et al. (1977) demonstrated refractori¬ ness to TSH of thyroid protein kinase, glucose oxidation and phospholipid synthesis. Rapoport 8c Adams (1976) showed refractoriness to TSH of thyroid cAMP response in cultured thyroid cells. Furthermore, recently Field et al. (1979) reported refractoriness to TSH of iodine organification in vitro and thyroid hormone secretion in vivo. Thus, refractoriness to TSH is a well-known pheno¬ menon and is supposed to be physiologically im¬ portant in controlling thyroid function to stimula¬ tion with TSH.

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Inhibition of thyroid-stimulating hormone stimulation of protein kinase, glucose oxidation, and phospholipid synthesis in thyroid slices previously exposed to the hormone.

Cited by 39 publications

References 21 publications

Role of the Hypothalamic TRH in the Regulation of Its Own Receptors in Rat Anterior Pituitaries

Role of the Hypothalamic TRH in the Regulation of Its Own Receptors in Rat Anterior Pituitaries

Lack of desensitization of 3',5'-cyclic AMP response to thyrotropin stimulation in differentiated thyroid carcinoma

Lack of refractoriness to stimulation with long acting thyroid stimulator of thyroid hormone synthesis and thyroid hormone secretion in mice in vivo

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