Stimulation of thyroidal iodothyronine 5'-monodeiodinase by long-acting thyroid stimulator (LATS)

1987 ◽  
Vol 114 (2) ◽  
pp. 193-200 ◽  
Author(s):  
Sing-Yung Wu ◽  
R. Reggio ◽  
W. Florsheim ◽  
I. J. Chopra ◽  
D. H. Solomon
Keyword(s):  
Marked Reduction ◽  
Maximum Velocity ◽  
Normal Serum ◽  
Detectable Change ◽  
Thyroid Glands ◽  
Long Acting ◽  
Insight Into ◽  
Stimulation Of ◽  
Mouse Thyroid

Abstract. To evaluate the effect of long-acting thyroid stimulator (LATS) on thyroid iodothyronine monodeiodinating activity, we have studied the in vitro conversion of T4 to T3 by mouse thyroid homogenate comparing tissue from LATS treated (0.1 ml LATS(+) serum, ip, for 3 days) with tissues from LATS(–) Graves' disease patients' serum or normal serum treated controls. Five out of seven LATS(+) sera were shown to stimulate the T4 5'-deiodinase significantly in mouse thyroid. There was no significant correlation between LATS titre and deiodinase activities in the different sera tested. To compare the effect of LATS and TSH (0.2 IU, ip daily), studies were carried out from 12 to 72 h. LATS had a similar latency of 12 h on the stimulation of thyroid deiodinase compared to TSH as reported earlier. However, the conversion activities reached a plateau by 12 h after LATS treatment, while it continued to rise upon daily TSH injection from 24 to 72 h. In addition, TSH caused a marked reduction of thyroid protein and an early peaking in serum T3 and T4 at 12 h, whereas LATS caused no detectable change in thyroid protein and a gradual rise in circulating T3 and T4. The kinetic analysis indicated that LATS-mediated stimulation of T4 5'-deiodinase was, similar to TSH, associated with an increase in maximum velocity (Vmax were 139, 208 and 505 pmol/mg protein/30 min respectively in control, LATS and TSH-treated animals) without a demonstrable change in the apparent Km (approximately 2.0 μm for T4). The present study demonstrated that some LATS-rich sera stimulate thyroid T4 to T3 conversion in mouse. It provides an insight into the mechanism of increased T3 secretion from Graves' thyroid glands.

A NEW IN VITRO ASSAY FOR THYROIDSTIMULATING HORMONE

1967 ◽  
Vol 38 (4) ◽  
pp. 439-449 ◽  
Author(s):  
JILL BROWN ◽  
D. S. MUNRO
Keyword(s):  
Radioactive Iodine ◽  
Thyroid Stimulating Hormone ◽  
Vitro Assay ◽  
Line Parallel ◽  
Thyroid Glands ◽  
Long Acting ◽  
Response Line ◽  
Mouse Thyroid

SUMMARY A new in vitro assay for thyroid-stimulating hormone (TSH) is described. The parameter of TSH action is the discharge of radioactive iodine from mouse thyroid glands labelled with 131I in vivo. The assay is sensitive to human TSH and gave consistent results during 1 yr. without seasonal variation. A potent preparation of long-acting thyroid stimulator gave a dose-response line parallel with human TSH. Fresh human serum was toxic to the assay preparation so that circulating TSH levels cannot be measured.

EFFECT OF ACTINOMYCIN D ON TSH-INDUCED STIMULATION OF THYROIDAL PROTEIN SYNTHESIS IN THE RAT

1974 ◽  
Vol 77 (1) ◽  
pp. 64-70 ◽  
Author(s):  
Gustav Wägar
Keyword(s):  
Protein Synthesis ◽  
Actinomycin D ◽  
The Other ◽  
Leucine Incorporation ◽  
Short Term ◽  
Other Hand ◽  
Thyroid Glands ◽  
Translational Level ◽  
Stimulation Of

ABSTRACT Whether the short-term regulation of thyroidal protein synthesis by TSH occurs at the transcriptional or the translational level was tested by measuring the effect of actinomycin D (act D) on the TSH-induced stimulation of L-14C-leucine incorporation into the thyroidal proteins of rats. TSH was injected 6 h before the rats were killed. The thyroid glands were then removed and incubated in vitro in the presence of L-14C-leucine for 2 h. The pronounced stimulation of leucine incorporation in the TSH-treated animals was depressed as compared with controls but still significant even when the animals had been pre-treated with 100 μg act D 24 and 7 h before sacrifice. On the other hand, act D strongly decreased incorporation of 3H-uridine into RNA. Short-term regulation of thyroidal protein synthesis by TSH appears to be partly but not wholly dependent on neosynthesis of RNA. Hence regulation may partly occur at the translation level of protein synthesis.

Hyperpolarization of thyroid cells in vitro by thyrotropin and cyclic AMP

1976 ◽  
Vol 231 (1) ◽  
pp. 52-55 ◽  
Author(s):  
R Batt ◽  
JM McKenzie
Keyword(s):  
Cyclic Amp ◽  
Short Term ◽  
Thyroid Cells ◽  
Low Concentrations ◽  
Thyroid Glands ◽  
The Relationship ◽  
Effect Of Feeding ◽  
Mouse Thyroid

With the use of microelectrodes, membrane potential (MP) was measured in mouse thyroid glands in vitro. A basal resting MP of about -39 mV was confirmed. The initial effect of feeding a low-iodine diet (6-12 days) was hyperpolarization, up to -47 m V; chronic low-iodine diet led to depolarization. Low concentrations of thyrotropin (less than 3 mU/ml superfusate) caused hyperpolarization and high ones (greater than 10 mU/ml) led to depolarization. Cyclic AMP (10(-3) M), dibutyryl cyclic AMP (1.2 X 10(-4) M or 1.2 X 10(-3) M) and theophylline (10(-2) or 10(-3) M) caused similar hyperpolarization: D- and DL-propranolol (5 X 10(-5) -5 X 10(-4) M) produced depolarization and inhibited hyperpolarization by thyrotropin. Conclusions are that hyperpolarization is a consequence of short-term increased secretion of thyrotropin in vivo or of low (near physiological) concentrations in vitro; these effects are probably mediated by cyclic AMP. The relationship to and mechanism of depolarization resulting from chronic enhanced endogenous secretion or high in vitro concentrations of thyrotropin are unknown.

ADENYL CYCLASE ACTIVITY IN THE MOUSE THYROID GLAND

1972 ◽  
Vol 52 (3) ◽  
pp. 533-540 ◽  
Author(s):  
PAT KENDALL-TAYLOR
Keyword(s):  
Inhibitory Effect ◽  
Thyroid Stimulating Hormone ◽  
Adenyl Cyclase ◽  
Human Thyroid ◽  
Intact Mouse ◽  
Adenyl Cyclase Activity ◽  
Thyroid Glands ◽  
Long Acting ◽  
Rate Of Activation ◽  
Mouse Thyroid

SUMMARY The activation of adenyl cyclase in intact mouse thyroid glands was measured by the conversion of [3H]ATP to [3H]cyclic AMP. Untreated serum had an inhibitory effect. Human thyroid-stimulating hormone (TSH) and γG-globulin prepared from serum containing the long-acting thyroid stimulator (LATS), activated adenyl cyclase and the log-dose—response relationship did not deviate from parallelism. The rate of activation by LATS was slower and the peak response was delayed, compared with the response to TSH. The possible significance of this is discussed. Other hormones and neurotransmitters examined had no effect on thyroidal adenyl cyclase.

A COMPARISON OF THE IN-VITRO ACTIONS OF THYROID-STIMULATING HORMONE AND CYCLIC 3′,5′-ADENOSINE MONOPHOSPHATE ON THE MOUSE THYROID GLAND

1969 ◽  
Vol 43 (3) ◽  
pp. 477-485 ◽  
Author(s):  
JANICE M. ENSOR ◽  
D. S. MUNRO
Keyword(s):  
Cyclic Amp ◽  
Culture Medium ◽  
Adenosine Monophosphate ◽  
Thyroid Stimulating Hormone ◽  
Vitro Assay ◽  
Thyroid Glands ◽  
Influence Of Tsh ◽  
Mouse Thyroid ◽  
Stimulating Hormone

SUMMARY In the in-vitro assay of Brown & Munro (1967) thyroid-stimulating hormone (TSH) increased the release of radioactive iodine from mouse thyroid glands labelled with 131i during life. Paper chromatography showed that TSH increased the 131I-labelling of thyroxine and tri-iodothyronine both in the culture medium and in hydrolysates of the thyroids. Cyclic 3′,5′-adenosine monophosphate (cyclic AMP) also increased 131I release in this assay and increased the 131I-labelling of thyronines in the culture medium. The effects on thyroid hydrolysates were less striking. Theophylline potentiated the influence of TSH and cyclic AMP in the assay and, by itself, increased 131I release and the labelling of iodothyronines in the thyroid without altering the distribution of 131I in the culture medium. The implications of these results are discussed.

Effects of in vivo triiodothyronine and long acting thyroid stimulator (LATS) administration on the in vitro thyroid cAMP response to thyrotrophin and LATS

1984 ◽  
Vol 106 (2) ◽  
pp. 193-198 ◽  
Author(s):  
Hitoshi Ikeda ◽  
Shoo Cheng Chiu ◽  
Nobuaki Kuzuya ◽  
Hidemasa Uchimura ◽  
Shigenobu Nagataki
Keyword(s):  
Drinking Water ◽  
Combined Treatment ◽  
Inhibitory Effects ◽  
Wet Weight ◽  
Per Se ◽  
Thyroid Hormone Levels ◽  
Long Acting ◽  
Mouse Thyroid

Abstract. The present study was undertaken to examine the effects of prolonged in vivo treatment with T3 and long acting thyroid stimulator (LATS) on in vitro responsiveness of mouse thyroid cyclic AMP to thyrotrophin (TSH) and LATS-immunoglobulin G (IgG). In control mice, thyroid cAMP concentrations after incubation with normal-IgG (10 mg/ml) for 2 h. TSH (10 mU/ml) for 10 min and LATS-IgG (10 mg/ml) for 2 h were 1.25 ± 0.11 (mean ± se) (n = 5), 15.87 ± 3.47 (n = 6) and 2.17 ± 0.25 pmoles/mg wet weight (n = 6), respectively. In mice given T3 (5 μg/ml in drinking water for 5 days, thyroid cAMP concentrations after an incubation with TSH were reduced by 50%, as compared to those of the control mice. They were also decreased in mice injected ip with 5 mg of LATS-IgG (1000%/5 mg in the McKenzie bioassay) daily for 5 days. Combined treatment with T3 and LATS decreased the cAMP response to TSH only to the same extent as did T3 alone, indicating that the inhibitory effects of T3 and LATS were not additive. Similar findings were observed with the thyroid cAMP response to LATS-IgG in vitro; either T3 or LATS treatment in vivo decreased cAMP response to LATS-IgG in vitro, but combined treatment with T3 and LATS did not cause further inhibition as compared with T3 or LATS treatment alone. These results indicate, 1) that prolonged in vivo T3 treatment inhibits the in vitro thyroid cAMP response not only to TSH but also to LATS-IgG, 2) that prolonged in vivo LATS treatment also suppresses the thyroid cAMP response both to TSH and LATS-IgG and 3) that the inhibitory effects of LATS may not be due to the effects of LATS per se but to increases in circulating thyroid hormone levels induced by prolonged LATS treatment.

The Influence of Adrenergic Receptor Blocking Agents on the Mouse Thyroid

1970 ◽  
Vol 39 (6) ◽  
pp. 781-791 ◽  
Author(s):  
Pat Kendall-Taylor ◽  
D. S. Munro
Keyword(s):  
Adrenergic Receptor ◽  
Adenosine Monophosphate ◽  
Thyroid Stimulating Hormone ◽  
Adrenergic Blockade ◽  
Blocking Drug ◽  
Receptor Blocking ◽  
Long Acting ◽  
Adrenergic Blocking ◽  
Mouse Thyroid

1. The influence of adrenergic receptor blocking drugs on the mouse thyroid gland maintained in vitro has been investigated. 2. Phentolamine, an α adrenergic blocking drug, and propranolol, a β blocking drug, inhibited the release of [131I]iodothyronines from pre-labelled mouse thyroids, which otherwise occurred when the glands were incubated in the presence of thyroid stimulating hormone, long acting thyroid stimulator, or cyclic 3′5′-adenosine monophosphate. 3. Evidence is presented to show that (a) the inhibition is not due to adrenergic blockade, (b) the effect cannot wholly be attributed to the prevention of adenyl cyclase activation, (c) the mechanism of action of the two drugs is dissimilar. 4. The observed clinical response in the treatment of thyrotoxicosis does not appear to be related to this antithyroid effect of propranolol.

ROLE OF THE HETEROGENEITY OF THYROGLOBULIN IN THE SECRETION OF THYROID HORMONE IN MICE

1980 ◽  
Vol 86 (3) ◽  
pp. 413-418 ◽  
Author(s):  
N. BAGCHI ◽  
T. R. BROWN ◽  
B. SHIVERS ◽  
R. E. MACK
Keyword(s):  
Drinking Water ◽  
Chromatographic Analysis ◽  
Hormone Secretion ◽  
Hormone Release ◽  
Basal Rate ◽  
Thyroid Glands ◽  
Hydrolysis Of ◽  
Mouse Thyroid

The rates of thyroglobulin hydrolysis and iodothyronine release from mouse thyroid glands were studied in vitro. Recently iodinated thyroglobulin ('new pool') had been labelled during life by injection of 131I 3 h before removal of the thyroid, 'old pool' thyroglobulin had been labelled by the administration of 125I in the drinking water for 1 week starting 3 weeks earlier. Chromatographic analysis of pronase digests of the thyroid glands showed that the iodothyronine content of the old and new pools were 19·5 and 7·4 per cent respectively. In the basal state the rate of thyroglobulin hydrolysis was lower from the old pool but the rate of hormone secretion was similar from both pools. Thyrotrophin (TSH) increased the rate of thyroglobulin hydrolysis and hormone release from both pools by up to four to six times the basal rate, the effect being maximal 2 h after administration of TSH and lasting for 6–8 h. The rate of thyroglobulin hydrolysis after TSH was similar in both pools but the rate of release of labelled iodothyronines was significantly higher from the old pool. These studies have indicated that although hydrolysis of thyroglobulin proceeds faster in the new pool than in the old ('last come, first served' hypothesis) nevertheless there is no difference in the rate of hormone secretion from the two pools, and hydrolysis in both pools is affected by TSH.

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