Inhibition of the Response of Mouse Thyroid to Thyrotropin Induced by Chronic Triiodothyronine Treatment

Gafni, Mikhal; Sirkis, Nava; Gross, J.

doi:10.1210/endo-97-5-1256

Cited by 33 publications

(13 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Therefore an explanation comprising the activity of the thyroid gland and h-TSH, HCG and human chorionic TSH effects is more likely in agreement with our observations (Braunstein and Hershman, 1976). The diminished response of T4 and cAMP to TSH in thyroid tissue pretreated with T3, as shown by Gafni et al (1975), as well as the FSHdependent thyroid cAMP release to the plasma (Ahren et al, 1978), are possible explanations for the findings, but not sufficiently proven.…”

Section: Commentsupporting

confidence: 52%

Plasma cAMP in Normal and Abnormal Human Pregnancy

Göser¹,

Jaschonek²,

Kindler³

et al. 1980

Gynecol Obstet Invest

View full text Add to dashboard Cite

Plasma cAMP was determined using the method of Toveyetal. in normal pregnant women with a mean concentration of 18.9 ± 0.8 pmol/ml (x ± SEM). Between weeks 9–12 and 33–36 of gestation, there were two peaks, with a mean cAMP of 22.5 ± 2.4, which were significantly increased in comparison to the other weeks of pregnancy. Significantly decreased values were found in patients with threatened abortion (weeks 12–28) which terminated in abortion (11.6 ± 2.4; p < 0.01). In premature labor no differences were found. During therapy with fenoterol there were highly significantly increased plasma cAMP levels (48.2 ± 2.8; p < 0.0005). During thyroid hormone therapy in euthyroid goiter, cAMP was significantly decreased (14.0 ± 1.4; p < 0.05). 1 week after cessation of therapy a highly significant increase of cAMP was observed (38.2 ± 6.9; p < 0.0005). There was a negative linear regression between T₃ and cAMP ( 2p < 0.01). In pregnancy with hypertension cAMP was significantly elevated (30.5 ± 3.8; p < 0.0005), but nearly normal under antihypertensive therapy. In pregnancy with edema only, no difference was found. Induction of labor with PGE₂_Α was followed by a decrease of plasma cAMP.

show abstract

Section: Commentsupporting

confidence: 52%

Plasma cAMP in Normal and Abnormal Human Pregnancy

Göser¹,

Jaschonek²,

Kindler³

et al. 1980

Gynecol Obstet Invest

View full text Add to dashboard Cite

show abstract

“…Release of T4, T3, or iodide induced by TSH might contribute to the refractoriness related to organification of iodide. Such a short-loop feedback system has been reported both in vivo and in vitro (13)(14)(15) but has also been denied in vivo (16). In the present experiments, thyroid hormones did not diminish the TSH stimulation of organification of iodide (Fig.…”

Section: Resultssupporting

confidence: 61%

In Vitro and In Vivo Refractoriness to Thyrotropin Stimulation of Iodine Organification and Thyroid Hormone Secretion

Field¹,

Dekker²,

Titus³

et al. 1979

J. Clin. Invest.

View full text Add to dashboard Cite

A B S T R A C T Earlier studies indicated that initial exposure of thyroid slices to thyrotropin diminished responsiveness of the adenylate cyclase-cyclic AMP system, glucose oxidation, and 32Pi incorporation into phospholipids upon readdition of the hormone. The present studies demonstrate that slices from dog, beef, and human thyroid glands initially incubated with thyrotropin (TSH) were less responsive to subsequent addition of the hormone when organification of iodide was examined. Increasing the amount of TSH did not overcome the refractoriness induced by the initial exposure to the hormone. Furthermore, the stimulatory effects of dibutyryl cyclic AMP and prostagladin E1 were abolished in slices previously incubated with TSH. Development of such refractoriness did not depend upon new protein synthesis and was not abolished by 1 mM prophylthiouracil in the first incubation. Addition of 0.1 ,uM thyroxine or triiodothyronine or 1.5 ,M iodide during all three incubations did not modify the response to TSH, added for the first time in the third incubation. However, 1 mM iodide in the buffer during all three incubations inhibited the response to TSH during the third incubation. During the refractory period, effects of TSH on colloid droplet formation were also diminished. The in vivo effect of TSH on serum 1-triiodothyronine in rats was significantly reduced when the rats had been injected with TSH 8 h earlier. These studies demonstrate that TSH-induced refractoriness also includes effects on organification of iodine and secretion of thyroid hormone. The results cannot be adequately explained by unresponsiveness of adenylate cyclase because effects of dibutyryl cyclic AMP and prostagladin E1 were also inhibited by prior exposure to TSH.

show abstract

“…In mice experiments in vivo, [8] TSH was unable to induce thyroidal refractoriness to TSH but restored responsiveness to TSH from the partial refractory state provoked by previous treatment with triiodothyronine. The results suggested that the prolonged absence of an adequate level of TSH might be the cause of thyroidal unresponsiveness to acute TSH administration.…”

Section: Discussionmentioning

confidence: 90%