The effect of thyroxin in thyroidectomized rats treated with methylthiouracyl

Andik, I; Balogh, L; Donhoffer, S

doi:10.1007/bf02166910

Cited by 12 publications

(6 citation statements)

References 8 publications

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“…This extrathyroidal action is independent of the first effect (14). The inhibition of peripheral deiodination is associated with a decrease in the biologic effectiveness of administered T4 as measured by a decrease in metabolic rate or induction of oxidative enzymes in vivo (15)(16)(17)(18)(19)(20) and in vitro (21)(22)(23) and an increase in thyrotropin (TSH) secretion (24)(25)(26)(27)(28). The thiocarbamide drugs that decrease To deiodination are the ones that also decrease its metabolic effectiveness (14).…”

Section: Introductionmentioning

confidence: 99%

“…The PTU-induced decrease in the peripheral deiodination of T4 to T3 has been shown to be associated with a decrease in biologic activity of T4 in vivo (15)(16)(17)(18)(19)(20) and in vitro (21)(22)(23). Methimazole and other thiocarbamide drugs which do not affect the deiodination of To do not interfere with its metabolic effectiveness (14).…”

Section: Introductionmentioning

confidence: 99%

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Propylthiouracil blocks extrathyroidal conversion of thyroxine to triiodothyronine and augments thyrotropin secretion in man.

Geffner¹,

Azukizawa²,

Hershman³

1975

J. Clin. Invest.

188

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A B S T R A C T Propylthiouracil (PTU) inhibits peripheral deiodination of thyroxine (T4) and triiodothyronine (T3) and decreases the metabolic effectiveness of T4 in animals. To assess the effect of PTU on extrathyroidal conversion of T4 to Ta in man, 15 studies were performed in 7 athyreotic patients treated with 100 or 200 Ag of L-T4 daily for 1 mo before the addition of PTU, 250 mg every 6 h for 8 days. Serum T3, T4, and thyrotropin (TSH) were measured daily by radioimmunoassay; serum TSH response to 500-ig thyrotropin-releasing hormone (TRH) was measured before and on the last day of giving PTU.On the 100-Ag L-T4 dose, serum T3 fell from 120±5 The data suggest that PTU blocks extrathyroidal conversion of To to Ts, thus increasing pituitary TSH secretion and augmenting the TSH response to TRH.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Propylthiouracil blocks extrathyroidal conversion of thyroxine to triiodothyronine and augments thyrotropin secretion in man.

Geffner¹,

Azukizawa²,

Hershman³

1975

J. Clin. Invest.

188

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“…Thus, in rats PTU and many related thiouracil-type compounds reduce the capacity of a given dose of T4 to increase the oxygen consumption of the whole animal (1)(2)(3)(4)(5)(6) and isolated tissues (7,8), to raise the activity of mitochondrial alpha glycerophosphate dehydrogenase (a-GPD) in heart, liver, and kidney (5,(8)(9)(10), to inhibit the pituitary release of TSH (7,(11)(12)(13)(14), and to decrease the heart rate (15). The peripheral tissue effects of PTU have been attributed to the capacity of this drug to inhibit T, deiodination (7,(15)(16)(17)(18)(19)(20).…”

Section: Introductionmentioning

confidence: 99%

Propylthiouracil inhibits the conversion of l-thyroxine to l-triiodothyronine

Oppenheimer¹,

Schwartz²,

Surks³

1972

J. Clin. Invest.

265

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A B S T R A C T 6-n-propylthiouracil (PTU) administered to male Sprague-Dawley rats maintained on 2 and 5 Ag L-thyroxine (T4)/100 g body weight resulted in a marked reduction in the rate of conversion of L-thyroxine to L-triiodothyronine (Ts). These effects could not be ascribed to induced hypothyroidism since the group maintained on 5 *g T4/day had normal levels of liver mitochondrial alpha glycerophosphate dehydrogenase. In confirmation of previous studies, PTU also reduced the fractional rate of deiodination of T&. These observations provide a possible explanation of the many published observations indicating that PTU antagonizes the tissue effects of T4 but not of T3. The data suggest that monodeiodination of To but not of T8 is essential before hormonal effects can be manifested at the cellular level.

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“…The rate of turnover of triiodothyronine and its physiological activity per mole of iodine are quite different from those of thyroxine (11). Furthermore, although the deiodination of thyroxine was inhibited by several goitrogens (12), and its hormonal action was less when these goitrogens were given (13,14), the hormonal action of triiodothyronine was little affected (15). Therefore, under certain conditions, it seems inappropriate to expect the PBI to reflect the thyrotropin response.…”

mentioning

confidence: 80%

An Essential Role of Thyroxine and Triiodothyronine Balance in Establishing Normal Pituitary-Thyroid Feedback Control in Goitrogen-Treated Rats

Yamada

Lewis

1968

Endocrinology

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Rats were fed propylthiouracil (0.05 %), methimazole (0.05 %), or sulfaguanidine (1 %) and injected with graded doses of thyroxine (0.5-3.0 jug) daily for 2 weeks. In spite of the high serum PBI with doses of 1.0 and 1.5 jug of thyroxine, goiter was still observed in animals fed propylthiouracil. Goiter was prevented only when the PBI was increased to 2.2 times that of the control level by giving 2.0 jug of thyroxine. Similar effects were found with methimazole and sulfaguanidine. In animals which were thyroidectomized and given thyroxine, methimazole slightly elevated the serum PBI and reduced the urinary excretion of radioiodine after a single injection of labeled thyroxine. However, since sulfaguanidine was without effect in these respects, the development of goiter in the presence of a high serum PBI cannot be explained by assuming that all 3 goitrogens interfered with the deiodination of thyx'oxine. On the other hand, goiter was prevented in propylthiouracil-fed animals by doses of thyroid powder which resulted in a serum PBI lower than normal. Furthermore, goiter prevention in methimazolefed animals was achieved by administering a mixture of triiodothyronine (0.1 jug) and thyroxine (1.0 /xg) which produced a normal serum PBI and thyrotropin level. Since normally triiodothyronine plays an important physiologic role, it is suggested that goiter could not be prevented without giving a dose of thyroxine that would elevate the serum PBI to compensate for the activity of triiodothyronine. The existence of a homeostatic relation between the level of serum PBI and thyrotropin secretion by the anterior pituitary can be shown in goitrogentreated animals only when an appropriate mixture of triiodothyronine and thyroxine is administered. (Endocrinology 82: 91, 1968) AS FIRST formulated by Aron et al.(1) J\. and then reiterated by Hoskins (2), it is generally held that the pituitarythyroid axis offers an example of a physiologic servomechanism. When the titer of circulating thyroxine rises, the anterior pituitary is selectively inhibited, and thereby the output of thyrotropin falls. On the other hand, episodic or persistent decrease of circulating thyroxine results in an increased secretion of thyrotropin. Since probably over 90% of the iodine in blood is represented by thyroxine (3-5), it has been suggested that the level of thyroxine, measured as PBI, may regulate the secretion of thyrotropin. Although most

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The effect of thyroxin in thyroidectomized rats treated with methylthiouracyl

Cited by 12 publications

References 8 publications

Propylthiouracil blocks extrathyroidal conversion of thyroxine to triiodothyronine and augments thyrotropin secretion in man.

Propylthiouracil blocks extrathyroidal conversion of thyroxine to triiodothyronine and augments thyrotropin secretion in man.

Propylthiouracil inhibits the conversion of l-thyroxine to l-triiodothyronine

An Essential Role of Thyroxine and Triiodothyronine Balance in Establishing Normal Pituitary-Thyroid Feedback Control in Goitrogen-Treated Rats

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