Thyroid Secretionin Vitro: Inhibition of TSH and Dibutyryl Cyclic-AMP Stimulated131I Release by Li+1

Williams, John A.; Berens, Stephen C.; Wolff, J.

doi:10.1210/endo-88-6-1385

Cited by 81 publications

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“…Glucose oxidation was measured in dog thyroid slices (approximately 50 mg) by incubating them with 0.5 uCi of [1-'4C]glucose and collecting the 14CO2 as described earlier (4). Colloid droplet formation was measured in vitro in mouse thyroids attached to the trachea (5). In vivo thyroid stimulating activity was measured by the method of McKenzie (6) and LH activity was measured by the method of Parlow (7).…”

Section: Methodsmentioning

confidence: 99%

The Contribution of Subunits of Thyroid Stimulating Hormone to the Binding and Biological Activity of Thyrotropin

Wolff

Winand

Kohn

1974

Proc. Natl. Acad. Sci. U.S.A.

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Section: Methodsmentioning

confidence: 99%

The Contribution of Subunits of Thyroid Stimulating Hormone to the Binding and Biological Activity of Thyrotropin

Wolff

Winand

Kohn

1974

Proc. Natl. Acad. Sci. U.S.A.

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“…Lazarus et al 1981). Lithium has been found to inhibit TSH-stimulated thyroid hormone release from thyroid tissue in vitro (Williams et al 1971, Mori et al 1989. Lithium-induced resistance to TSH can be demonstrated in pig thyroid cells where 1 mM inhibits TSH-stimulated cAMP accumulation within 30 min (Wragg & Mac Neil 1991).…”

Section: Introductionmentioning

confidence: 99%

Differential effect of thyroid-stimulating hormone (TSH) on intracellular free calcium and cAMP in cells transfected with the human TSH receptor

Metcalfe¹,

Findlay²,

Robertson³

et al. 1998

Journal of Endocrinology

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The thyroid-stimulating hormone (TSH) binds to a receptor which activates adenylate cyclase and elevates cAMP concentration. In addition, effects of TSH on intracellular calcium and inositol phosphate accumulation have been reported. However, the mechanism of TSH-stimulated accumulation of inositol phosphates and elevation of calcium levels is unresolved. Previous work from this laboratory has shown TSH to cause acute transient increases in intracellular calcium in pig, human and FRTL-5 rat thyroid cells as well as in cells transfected with the human TSH receptor ( JPO9 cells) in some (but not all) experiments. The aim of this study was to investigate the variability of the calcium response to TSH in JPO9 cells to learn more about the nature of this calcium signal induction. Calcium responses to TSH were determined using the fluorochrome fura-2 in both monolayers of adherent cells and adherent single cells. The responses to a single addition and to repetitive additions of TSH were compared. We also determined the cAMP response to TSH using these two protocols of TSH addition.Our data show that, whereas the cAMP response to TSH is highly predictable and consistent and does not require multiple exposures to TSH, cells were unlikely to respond to TSH with an increase in calcium unless they received multiple challenges with the hormone. A single addition of 10 mU/ml TSH failed to increase calcium in any of 40 single cells examined and in only 4 of 15 monolayers of cells (27%) examined; in contrast, 10 of 12 monolayers eventually responded with an increase in calcium after multiple exposure to TSH and 18 of 67 single cells. Similar data were obtained whether calcium was measured in single cells or in populations of cells. We also demonstrated cooperativity between an adenosine derivative, N 6 -(-2-phenylisopropyl)adenosine, and TSH such that their co-administration resulted in a consistent and marked elevation in calcium levels not achieved with either agonist alone. In summary, we suggest that the coupling between the TSH receptor and the intracellular signalling system that leads to activation of intracellular calcium in JPO9 cells requires repetitive stimulation or the influence of other agonists, in contrast with the coupling between the TSH receptor and activation of the adenylate cyclase enzyme.

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“…Lithium inhibits the formation and release of thyroid hormone [1][2][3][4], and has produced hypothyroidism. However, lithium-induced thyrotoxicosis may also occur [5][6][7].…”

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confidence: 99%

“…Lithium carbonate alters thyroid function and has been reported to induce hypothyroidism [1][2][3][4]. Somewhat surprisingly, thyrotoxicosis has also been attributed to lithium administration [5][6][7].…”

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confidence: 99%

Acute Adrenal Insufficiency after Unilateral Adrenalectomy in Cushing's Syndrome: Precipitation by Lithium-Induced Thyrotoxicosis during Cortisol Replacement.

et al. 1994

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Thyroid Secretionin Vitro: Inhibition of TSH and Dibutyryl Cyclic-AMP Stimulated¹³¹I Release by Li⁺1

Cited by 81 publications

References 0 publications

The Contribution of Subunits of Thyroid Stimulating Hormone to the Binding and Biological Activity of Thyrotropin

The Contribution of Subunits of Thyroid Stimulating Hormone to the Binding and Biological Activity of Thyrotropin

Differential effect of thyroid-stimulating hormone (TSH) on intracellular free calcium and cAMP in cells transfected with the human TSH receptor

Acute Adrenal Insufficiency after Unilateral Adrenalectomy in Cushing's Syndrome: Precipitation by Lithium-Induced Thyrotoxicosis during Cortisol Replacement.

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