THE IN VITRO METABOLISM OF THYROXINE, TRIIODOTHYRONINE AND THEIR ACETIC AND PROPIONIC ACID ANALOGUES<sup>1</sup>

Yamazaki, Eiichi; Slingerland, D. Ward

doi:10.1210/endo-64-1-126

Cited by 38 publications

(11 citation statements)

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“…The depression in T 3 may be caused by an impairment in peripheral conver-sion of T 4 to T 3 . Enzymes that deiodinate thyroxine are found in both liver and kidney (Yamazaki and Slingerland, 1959). As the kidney was enlarged by the P deficiency, it is possible that damage to the kidney may have impaired the deiodination mechanism in this organ.…”

Section: Resultsmentioning

confidence: 99%

Thyroid Function, Growth Hormone, and Organ Growth in Broilers Deficient in Phosphorus

et al. 1987

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The effects of a dietary P deficiency on thyroid function, serum growth hormone, and growth parameters in 10 to 29-day-old broiler cockerels was determined. Chicks fed severely P-deficient diets (.05% or .10% available P) grew more slowly and ate less feed than controls fed .65% P. The deficiency was also accompanied by hypercalcemia, hypophosphatemia, and decreases in percent bone ash, fat-free tibial weight, and tibial length and width. Increases in the relative weights of kidneys, hearts, and pituitary glands (.05% P only) occurred as well. Most of these changes occurred to a lesser extent or not at all in pair-fed controls, showing that they resulted specifically from the P deficiency and were not simply a result of reductions in feed intake. Phosphorus deficiency also was accompanied by peripheral edema and hydropericardium. Relative thyroid weight was unaffected. Serum triiodothyronine was consistently lower in the P-deficient chicks, although effects were significant only in one experiment. Thyroxine levels tended to be low also, but not consistently so. Serum growth hormone in P-deficient chicks in both studies was consistently lower than that in pair-fed controls, but this was significant only when .10% but not .05% available P was fed. The findings suggest that serum levels of both thyroid hormone and growth hormone are altered by P deficiency, but the results were not clearly definitive.

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Section: Resultsmentioning

confidence: 99%

Thyroid Function, Growth Hormone, and Organ Growth in Broilers Deficient in Phosphorus

et al. 1987

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“…However, it is not known whether such effects on oxidative metabolism might result from or lead to changes in the intracellular metabolism of thyroxine. More direct efforts to evaluate this question have led to contradictory conclusions, since estrogens have had variable effects on the degradation of thyroxine by cellular preparations, in zvitro (28,29). Finally, in vzivo, estrone does not affect the disappearance of thyroxine from the plasma of rats or rabbits (30,31).…”

Section: Resultsmentioning

confidence: 99%

The Effect of Estrogens Upon the Peripheral Metabolism of Thyroxine *†

Dowling¹,

Freinkel²,

Ingbar³

1960

J. Clin. Invest.

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In plasma, thyroxine is avidly bound to specific proteins present in low concentration, particularly the so-called thyroxine-binding globulin (TBG) and thyroxine-binding pre-albumin (TBPA) (1-4). Several observations indicate that such protein-hormone interactions are of physiological importance. In vitro, the ability of cellular systems to accumulate thyroxine from suspending media is conditioned by the thyroxine-binding potency of the proteins within the media (5, 6). In addition, the volume of distribution and rate of turnover of thyroxine in vivo resemble those of certain plasma proteins (7, 8)'. Finally, abnormal thyroxine-binding by TBG and TBPA has been observed in a variety of states in which the peripheral metabolism of thyroid hormone is disturbed (9-12). It therefore seemed possible that interactions with plasma proteins might in part regulate the peripheral utilization and degradation of thyroxine.An ideal test of this hypothesis would be provided by studies of hormonal metabolism performed before and during the administration of large quantities of purified binding protein. However, adequate quantities of these materials are not yet available. Therefore, it. has been necessary to assess the effects of alterations in thyroxinebinding induced by pharmacological means. Large

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“…These in vivo observations, while consistent with the major hypothesis, have not been entirely conclusive because of the possibility that the agents employed might directly affect cellular mechanisms for the disposal of hormone. This seemed especially possible in the case of diethylstilbestrol, in view of reports that this compound inhibits the deiodination of T4 both by intact cellular preparations and by a partially purified thyroxine-deiodinase (19,20).…”

Section: Discussionmentioning

confidence: 99%

Clinical and Physiological Observations in a Patient With an Idiopathic Decrease in the Thyroxine-Binding Globulin of Plasma*

Ingbar¹

1961

J. Clin. Invest.

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THE IN VITRO METABOLISM OF THYROXINE, TRIIODOTHYRONINE AND THEIR ACETIC AND PROPIONIC ACID ANALOGUES¹

Cited by 38 publications

References 0 publications

Thyroid Function, Growth Hormone, and Organ Growth in Broilers Deficient in Phosphorus

Thyroid Function, Growth Hormone, and Organ Growth in Broilers Deficient in Phosphorus

The Effect of Estrogens Upon the Peripheral Metabolism of Thyroxine *†

Clinical and Physiological Observations in a Patient With an Idiopathic Decrease in the Thyroxine-Binding Globulin of Plasma*

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THE IN VITRO METABOLISM OF THYROXINE, TRIIODOTHYRONINE AND THEIR ACETIC AND PROPIONIC ACID ANALOGUES1

Cited by 38 publications

References 0 publications

Thyroid Function, Growth Hormone, and Organ Growth in Broilers Deficient in Phosphorus

Thyroid Function, Growth Hormone, and Organ Growth in Broilers Deficient in Phosphorus

The Effect of Estrogens Upon the Peripheral Metabolism of Thyroxine *†

Clinical and Physiological Observations in a Patient With an Idiopathic Decrease in the Thyroxine-Binding Globulin of Plasma*

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THE IN VITRO METABOLISM OF THYROXINE, TRIIODOTHYRONINE AND THEIR ACETIC AND PROPIONIC ACID ANALOGUES¹