The Action of Thyrotropin on Thyroid Metabolism

Dumont, Jacques Emile

doi:10.1016/s0083-6729(08)60051-5

Cited by 334 publications

(113 citation statements)

References 345 publications

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“…If it is generally accepted that chronic hyperstimulation by TSH is responsible for thyroid hypertrophy and hyperplasia (Dumont, 1971) there are indications that the TSH action is not sufficient to induce these processes (Jolin et al, 1974;Isler, 1974 (Fayet et al, 1982). We have shown that TSH also enhances the proliferation of canine thyroid cells cultured in a high serum medium .…”

Section: Discussionmentioning

confidence: 99%

Factors controlling proliferation and differentiation of canine thyroid cells cultured in reduced serum conditions: effects of thyrotropin, cyclic AMP and growth factors

Roger¹,

Dumont²

1984

Molecular and Cellular Endocrinology

199

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Section: Discussionmentioning

confidence: 99%

Factors controlling proliferation and differentiation of canine thyroid cells cultured in reduced serum conditions: effects of thyrotropin, cyclic AMP and growth factors

Roger¹,

Dumont²

1984

Molecular and Cellular Endocrinology

199

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“…Much evidence has been provided indicating that this effect of TSH is not mediated by the adenylate cyclasecyclic AMP system (7,20,21 Although these studies clearly demonstrate that unresponsiveness to TSH extends to other metabolic effects of the hormone in addition to generation of cyclic AMP, they do not provide unequivocal evidence that such refractoriness is of physiological significance or involved in the hormonal regulation of thyroid gland function.…”

Section: Discussionmentioning

confidence: 94%

“…I,-(I that the basis for refractoriness is more complex than unresponsiveness of adenylate cyclase. In dog thyroid slices, stimulation of glucose oxidation by TSH (7) and PGE, (15) (12,18). The stimulation of glucose oxidation by acetylcholine (14) was not inhibited in slices which were refractory to TSH.…”

Section: Discussionmentioning

confidence: 99%

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

Field¹,

Bloom²,

C³

et al. 1977

J. Clin. Invest.

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A B S T R A C T Prior exposure ofthyroid slices to thyrotropin (TSH) induced refractoriness to subsequent stimulation of the cyclic AMP system by the hormone. Although the inhibition is incomplete, we examined whether the reduction in cyclic AMP was sufficient to alter other metabolic effects of TSH. Bovine or dog thyroid slices were incubated with or without 5-100 mU/ml TSH for 1-2h, washed, and then incubated without hormone for 1-2 h. Half of the slices not exposed to TSH initially were then incubated with buffer and half were exposed to 5-100 mU/ml TSH. Slices initially incubated with TSH were also incubated with or without TSH in the third incubation. During the refractory period, TSH activation of protein kinase was inhibited even though the hormone still caused some increase in cyclic AMP concentrations. However, protein kinase activity was fully responsive to dibutyryl cyclic AMP when slices were incubated with it during the third incubation. Stimulation of glucose oxidation by TSH was significantly decreased in thyroid slices previously incubated with the hormone. During refractoriness, stimulation of glucose oxidation caused by prostaglandin E1 and dibutyryl cyclic AMP was also significantly diminished but that due to acetylcholine was not. Thus even though dibutyryl cyclic AMP could fully activate protein kinase activity during refractoriness, its effect on glucose oxidation was still inhibited, suggesting that the metabolic block responsible for this refractoriness was distal to activation of protein kinase. Stimulation of 32P, incorporation into phospholipid by TSH and acetylcholine was Received for publication 23 August 1976 and in revised form 29 November 1976. also inhibited during refractoriness. Despite reduction of the stimulatory effect of TSH, binding of 125I1 TSH was not modified by prior incubation of thyroid slices with TSH. These results indicate that changes in the TSH receptor are not responsible for the development of refractoriness and other metabolic sites besides activation of adenylate cyclase appear to be involved.

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“…The importance of prostaglandins (PGs) in the thyroid physiology has been a controversial subject for many years but it is generally acknowledged that: (1) PGE compounds stimulate thyroid adenylate cyclase and cAMP synthesis [10,11 ] and iodine metabolism [10] and reproduce some of the effects of TSH in vitro [10] and PGI2 has similar effects on cAMP synthesis and iodine metabolism [21; (2) TSH stimulates PGI2 and PGE2 syntheses [3]. There have been proposed several hypotheses to connect these two, intending to find the role of PGs in the thyroid receptor-adenylate cyclase and cAMP system.…”

Section: Discussionmentioning

confidence: 99%

Increases of prostacyclin and PGE₂ levels after acute thyrotropin stimulation in cultured porcine thyroid cells

et al. 1981

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The Action of Thyrotropin on Thyroid Metabolism

Cited by 334 publications

References 345 publications

Factors controlling proliferation and differentiation of canine thyroid cells cultured in reduced serum conditions: effects of thyrotropin, cyclic AMP and growth factors

Factors controlling proliferation and differentiation of canine thyroid cells cultured in reduced serum conditions: effects of thyrotropin, cyclic AMP and growth factors

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

Increases of prostacyclin and PGE₂ levels after acute thyrotropin stimulation in cultured porcine thyroid cells

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The Action of Thyrotropin on Thyroid Metabolism

Cited by 334 publications

References 345 publications

Factors controlling proliferation and differentiation of canine thyroid cells cultured in reduced serum conditions: effects of thyrotropin, cyclic AMP and growth factors

Factors controlling proliferation and differentiation of canine thyroid cells cultured in reduced serum conditions: effects of thyrotropin, cyclic AMP and growth factors

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

Increases of prostacyclin and PGE2 levels after acute thyrotropin stimulation in cultured porcine thyroid cells

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Increases of prostacyclin and PGE₂ levels after acute thyrotropin stimulation in cultured porcine thyroid cells