Nonhormonal Iodine Escape from the Normal and Abnormal Thyroid Gland<sup>1</sup>

Ohtaki, Sachiya; Moriya, Shigeru; Suzuki, Hoji; Horiuchi, Yoshihiko

doi:10.1210/jcem-27-5-728

Cited by 21 publications

(5 citation statements)

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“…There has been an accumulating body of evidence both in man and in animals which indicates that there are two functional I-pools which serve as sources for new hormone formation (20)(21)(22)(23)(24). These pools are generally referred to as the first and second pool.…”

Section: Resultsmentioning

confidence: 99%

A new method for the measurement of thyroidal iodine release in man

Nicoloff¹

1970

J. Clin. Invest.

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ABSTRA CT A new method is described for the detection of variations in the release rate of all iodinated products by the thyroid gland in man. 'I was employed to endogenously label the thyroid gland, and a parenterally administered '81I thyroxine dose was used to generate a 181I reference source. Thyroidal iodine release activity was quantitatively assessed by the measurement of variations in 'I/I ratio values obtained in timed urine samples. Diurnal variation in thyroid release patterns was observed in euthyroid subjects which was promptly suppressed by exogenous triiodothyronine administration and was simulated by the intramuscular injection of 0.25-0.50 U of bovine thyrotropin. The zenith value occurred at 4:00 a.m. ±3.4 hr (SD) and the nadir at 5:00 p.m. ±3.6 hr. The absence of a diurnal pattern in patients with thyrotoxicosis and in secondary hypothyroidism indicated that this diurnal fluctuation was under thyrotropin (TSH) regulation. This new method also promises to be a useful tool for the study of the intrathyroidal recycling of iodide from the iodotyrosine pool and the detection of factors which may acutely alter thyroid function.

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Section: Resultsmentioning

confidence: 99%

A new method for the measurement of thyroidal iodine release in man

Nicoloff¹

1970

J. Clin. Invest.

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“…The thyroid gland rather tries to protect and recycle the immature Tg through a two-step transport system: first, through the Golgi compartment where novel oligosaccharides are added, followed by transport back to the follicular lumen where additional iodination and hormone formation occurs (2,6). Another fraction of the immature Tg molecules is transported via transcytotic vesicles to the basolateral thyrocyte membrane and then released into the bloodstream (2,31).…”

Section: Discussionmentioning

confidence: 99%

Genetic Variants in theST6GAL1Gene Are Associated with Thyroglobulin Plasma Level in Healthy Individuals

Matana

Popović

Boutin

et al. 2019

Thyroid

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Background: Thyroglobulin (Tg) is a 660 kDa iodoglycoprotein that serves as a scaffold for thyroid hormone synthesis. Although a twin study showed that variability of serum Tg levels has a substantial genetic basis, no genome-wide association study (GWAS) of serum/plasma Tg levels has been performed to date. The aim of this study was to identify genetic variants associated with plasma Tg levels among healthy individuals. Methods: A GWAS was conducted on two Croatian cohorts, and a combined analysis was performed. The analyses included 1094 individuals. A total of 7,597,379 variants, imputed using the 1000 Genomes reference panel, were analyzed for association. GWAS was performed under an additive model, controlling for age, sex, and relatedness within each data set. Combined analysis was conducted using the inverse-variance fixed-effects method. Results: Sixteen variants located on chromosome 3, within the ST6GAL1 gene, reached genome-wide significance. The lead SNP was rs4012172 (p ¼ 1:29 • 10 À 10), which explained 3.19% of the variance in Tg levels. ST6GAL1 belongs to the sialyltransferase protein family, which has a fundamental role in the synthesis of specific sialylated structures on various glycoproteins, including Tg. It is known that only immature Tg (poorly sialylated or desialylated) can be transferred to the bloodstream. Conclusions: A highly biologically plausible locus was identified that could have a role in the regulation of plasma Tg levels in healthy individuals.

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“…A number of studies indicate that release of thyroid iodine in a non-hormonal form is an important process during normal thyroid function and in a variety of thyroid diseases, including thyroiditis, congenital metabolic goitre, and thyrotoxicosis (DeGtoot 1966;Nagataki et al 1967;Ohtaki et al 1967;Fishet 8c Oddie 1964). Slingetland 8c Buttows (1962) compared the ratio of PB131I to urinary 131I, before and after administration of methimazole, in normal subjects and thyrotoxic patients.…”

mentioning

confidence: 99%

“…Ermans et al (1963) previously observed the same type of evidence for iodide leak in patients with endemic goitre. More recently, Ohtaki et al (1967) have noted evidence for release of non-hormonal iodide from the thyroid in subjects with »coast goitre« in Japan.…”

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confidence: 99%

Effect of Perchlorate and Methimazole on Iodine Metabolism

DeGroot

Bühler

1971

Acta Endocrinologica

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The increment in urinary iodide excretion was compared, in normal and thyrotoxic subjects, during the baseline state and after administration of potassium perchlorate or methimazole. In the normal subjects, perchlorate administration produced increments of urinary iodide that appear to be equivalent to hormonal iodine secretion per day. Urinary iodide excretion was increased to 2.2\p=n-\2.8fold this level by methimazole This result is interpreted as compatible with extensive intrathyroidal recirculation of iodotyrosine iodide and leakage of a small fraction of this iodide to the blood in normal subjects. In thyrotoxic subjects, the average increment in iodide excretion produced by perchlorate was 464 \g=m\g/day. Methimazole augmented urinary iodide excretion 2.2 fold the level found with perchlorate, indicating that there is extensive conservation of intrathyroidal iodide in thyrotoxicosis. The technique allows a qualitative estimation of efficiency of reutilization of intrathyroidal iodine.Potassium perchlorate blocks iodine transport into the thyroid through com¬ petitive inhibition of the iodide trapping mechanism (Wyngaarden et al. 1952). By preventing uptake of iodide from blood, it presumably should completely inhibit recirculation of iodide derived from degradation of thyroid hormone in peripheral tissues. Isaacs et al. (1966) report that in the dog perchlorate also causes a discharge of some iodide derived from intrathyroidal sources (pre¬ sumably from the deiodination of iodotyrosine). The extent of this discharge

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Nonhormonal Iodine Escape from the Normal and Abnormal Thyroid Gland¹

Cited by 21 publications

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A new method for the measurement of thyroidal iodine release in man

A new method for the measurement of thyroidal iodine release in man

Genetic Variants in theST6GAL1Gene Are Associated with Thyroglobulin Plasma Level in Healthy Individuals

Effect of Perchlorate and Methimazole on Iodine Metabolism

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Nonhormonal Iodine Escape from the Normal and Abnormal Thyroid Gland1

Cited by 21 publications

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A new method for the measurement of thyroidal iodine release in man

A new method for the measurement of thyroidal iodine release in man

Genetic Variants in theST6GAL1Gene Are Associated with Thyroglobulin Plasma Level in Healthy Individuals

Effect of Perchlorate and Methimazole on Iodine Metabolism

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Nonhormonal Iodine Escape from the Normal and Abnormal Thyroid Gland¹