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PubMed1976

Metabolism of thyroxine-binding globulin in man. Abnormal rate of synthesis in inherited thyroxine-binding globulin deficiency and excess.

It has been previously suggested that inherited thyroxine-binding globulin (TBG) abnormalities in man may be due to mutations at a single X-chromosome-linked locus controlling TBG synthesis. However, abnormalities in TBG degradation have not been excluded. The availability of purified human TBG and its successful labeling with radioiodide allowed us to examine such possibility. Human TBG was purified by affinity chromatography, labeled under sterile conditions with 131I or 125I,, and mixed with [125I]thyroxine (T4) or [131I]T4, respectively, before their intravenous injection. Blood and urine samples were collected over a 10-day period, and the turnover parameters were calculated. In eight normal volunteers mean values +/-SD for TBG and T4 respectively, were as follows: Half time (t1/2) 5.3 +/- 0.4 and 7.0 +/- 0.6 days; distribution space (DS) 7.2 +/- 1.0 and 10.8 +/- 1.2 liters; and total daily degradation (D) 0.211 +/- 0.053 and 0.088 +/- 0.011 mumol/day. In all subjects, t1/2 of TBG was shorter than that of T4; and the DS was smaller. 2.4 mol of TBG was degraded for each mole of T4. In five of six subjects from four families, comprising hemizygous and heterozygous carriers of TBG absence, decrease, and excess, the t1/2 and DS for TBG were within the normal range. The D of TBG was proportional to the serum concentration of the protein. Changes in the T4 kinetics in these patients were compatible with euthyroidism and with the known alterations in the extrathyroidal T4 pool associated with the changes in serum TBG concentration. A striking decrease in the t1/2 of TBG was found only in a patient with acquired diminution in TBG concentration and in patients with thyrotoxicosis or other conditions apparently unrelated to thyroid dysfunction. TBG t1/2 was 2.5 days in a patient with multiple myeloma and 3.6 days in two patients with thyrotoxicosis. Decreased TBG t1/2 was also observed in three of six patients with nonthyroidal pathology and was associated with an increase in TBG D disproportionate to their level of serum TBG. These studies indicate that changes in TBG concentration in patients with X-chromosome-linked TBG abnormalities are due to alterations in its rate of synthesis. In other conditions, abnormalities of TBG degradation and/or rate of synthesis may be found.

Adult↗
PubMed1977

A reassessment of 8-anilino-1-naphthalene sulphonic acid as a thyroxine binding inhibitor in the radioimmunoassay of thyroxine.

The effectiveness of 8-anilino-1-naphthalene sulphonic acid (ANS) in the radioimmunoassay (RIA) of thyroxine (T4) as an inhibitor of the binding of T4 to serum T4-binding proteins is assessed. The optimum ANS concentration is dependent upon the antiserum and the method used for separating free and bound T4. If T4 binding to serum proteins is not completely inhibited, resin separation methods may yield low values, while polyethylene glycol and double-antibody methods may produce high values for T4 concentration. Even with optimum ANS concentration gross errors in measurement of T4 may occur in patients with high thyroxine-binding globulin (TBG) concentrations.

Anilino Naphthalenesulfonates↗
PubMed1979

Effect of ACTH-stimulated glucocorticoid hypersecretion on the serum concentrations of thyroxine-binding globulin, thyroxine, triiodothyronine, reverse triiodothyronine and on the TSH-response to TRH.

The responses of serum concentrations of TSH, thyroxine (T4), triiodothyronine (T3) and of reverse triiodothyronine (rT3) to i. v. administration of 0.4 mg THR were examined prior to (and after) i. m. administration of ACTH (2 mg Synacthen Depot) in 7 euthyroid women using estrogen-containing oral contraceptives and in 8 controls, with the following results: (1) an increase in endogenous glucocorticoid secretion is associated with a depression of the TSH response to TRH; (2) TSH formed in decreased amounts is still capable of stimulating thyroid secretion; (3) the increased serum corticoid levels fail to affect the secretory response of the thyroid to TSH; (4) control of the pituitary-thyroid axis remains normal in the presence of increased serum thyroxine-binding globulin (TBG) levels. In a further series the serum levels of TBG, T4, T3, rT3 and cortisol under the effect of ACTH-induced endogenous glucocorticoid hypersecretion were studied in 6 normal untreated controls, in 6 normal women using oral contraceptives and in 10 untreated hyperthyroid patients. During four days subsequent to treatment the serum TBG levels decreased, maximum decrease being found in the users of oral contraceptives, minimum decrease in the controls. Serum T4 was found to decrease during 2 to 4 days, serum T3 parallel with an increase in serum rT3, for 1 to 2 days, subsequent for ACTH loading. In the euthyroid cases also the serum TSH levels showed a transitory decline. It is concluded that in case of endogenous hyperproduction of glucocorticoids (1) T4 leads to T3 monodeiodination decreases and T4 leads to rT3 conversion increases parallel with the changes in the serum cortisol levels; (2) TBG synthesis is inhibited by endogenous glucocorticoids; (3) the changes in serum TBG levels are accompanied by a decrease in the serum T4 concentrations.

Adrenocorticotropic Hormone↗
PubMed1977

Free thyroxine index or effective thyroxine ratio?

The ability of the free thyroxine index (FTI) and the effective thyroxine ratio (ETR) to distinguish abnormal from normal thyroid function is compared in a series of 422 patients; they were equally successful in detecting hyperthyroidism. In hypothyroidism, however, the ETR values of 22% were within 95% 'normal' limits compared with 7,4% of the FTI values. Other authors have shown a similar poorer sensitivity of the ETR compared with the FTI.

Humans↗
PubMed1979

Endocrinology of pregnancy. I. Denominations of concentrations of triiodothyronine, thyroxine, effective thyroxine, thyreotrophin and growth hormone in normal pregnancy, labour and in cord blood.

Concentrations and activities of the following agents were estimated: triiodothyronine (T3), thyroxine (T4), effective thyroxine (ETR), thyreotrophin (TSH), and growth hormone (HGH). Blood samples were collected in pregnancy, labour and from the umbilical cord of the newborns. It was demonstrated that in normal pregnancy the concentrations of T3, ETR, and TSH did not differ significantly from the values considered as normal in non-pregnant women. The concentration of T4 was distinctly higher in the course of pregnancy (139 to 157 nmol/l versus 110 nmol/l in non-pregnant subjects). The HGH concentration increased during pregnancy from 5.6 to 14.3 micrograms/l. The cord blood demonstrated comparable values of ETR and HGH and in half of the cases of TSH also with those observed in the mothers. In the other one half of the cases, TSH activity was fourtimes higher than the material value. The T3 and T4 were lower than values in the mothers. The results presented are the normal values for further planned investigations of endocrinology of pregnancy, especially for studies into course of pregnancy in women who work in noxious conditions.

Female↗
PubMed1979

Thyroxine uptake and metabolism by fetal sheep after intra-amniotic thyroxine injection.

Thyroxine (T4) uptake from amniotic fluid was investigated in fetal sheep. Samples of fetal and maternal blood and of amniotic fluid were obtained from indwelling catheters at specific intervals after intra-amniotic injection of T4. T4 and reverse T3 (rT3) were measured by radioimmunoassay. Basal levels of T4 were 7.3 +/- 0.92, less than 2, and 6.28 +/- 0.49 microgram/dl in the fetus, amniotic fluid, and ewe, respectively. Basal levels of rT3 were 3,858 +/- 214, 189 +/- 62, and 385 +/- 20 pg/ml in the fetus, amniotic fluid, and ewe, respectively. T4 and rT3 rose progressively in the fetus with maximum concentrations of 25 to 30 microgram/dl T4 by 10 hours and 11,000 to 14,000 pg/ml rT3 by 20 hours after intra-amniotic injection of 500 microgram of T4. These concentrations returned toward baseline by 50 and 70 hours for T4 and rT3, respectively. The increase of fetal T4 was proportional to the amount of T4 injected in a range of 250 and 2,500 microgram. Esophageal ligation abolished the changes in fetal T4 but not rT3. Amniotic fluid rT3 increased with time after intra-amniotic injection of T4 and returned to baseline long after amniotic fluid T4 had reached basal levels. This pattern persisted despite esophageal ligation. T4 was converted to rT3 during incubation in amniotic fluid in vitro. It is concluded that (1) substantial amounts of T4 are taken up by fetal fetal sheep from the amniotic fluid by deglutition, (2) increases in fetal concentrations of T4 and rT3 are related to the amount of T4 added to the amniotic fluid, (3) amniotic fluid and fetal rT3 concentrations increase following intra-amniotic injection of T4 in the absence of significant uptake of T4 by the fetus, and (4) significant amounts of T4 may be converted to rT3 in vitro during incubation of T4 in amniotic fluid.

Amnion↗
PubMed1979

Inhibition of intrapituitary thyroxine to 3.5.3'-triiodothyronine conversion prevents the acute suppression of thyrotropin release by thyroxine in hypothyroid rats.

Iopanoic acid has been shown to block thyroxine (T4)-5'-monodeiodination in rat anterior pituitary in vitro. To test the hypothesis that the acute decrease in thyrotropin (TSH) after infusion of T4 into hypothyroid rats requires intrapituitary T4 to 3,5,3'-triiodothyroxine (T3) conversion, the effect of iopanoic acid treatment on the generation of nuclear T3 from intrapituitary conversion and the response to TSH were compared in control and iopanoic acid-treated animals. 5 mg/100 g body weight iopanoic acid given 24, 16, and 1.5 h before administration of 125I-T4 reduced the quantity of pituitary nuclear 125I-T3 from local (intrapituitary) T4 to T3 conversion by 60-100%. In association with inhibition of intrapituitary T4 to T3 conversion, there was an increase in the binding of 125I-T4 to the nuclear receptor of the pituitary but the total iodothyronine content of the nuclei was still less than half of the nuclear iodothyronine in control animals. Iopanoic acid did not affect the nuclear/plasma ratio of injected 131I-T3 in the same animals, but did appear to impair 131I-T3 clearance or reduce its distribution volume. Treatment with iopanoic acid did not reduce the quantity of nuclear 125I-T3 in the liver, kidney, or heart of the same animals more than expected from the changes in serum 125I-T3. In control hypo-thyroid animals pretreated with iopanoic acid, the mean TSH was not significantly decreased from the initial value by T4 injection. Iopanoic acid pretreatment did not interfere with the acute TSH response of chronically hypothyroid rats to 70 ng of T3/100 g body weight. These results establish that intrapituitary generations of T3 from T4 is required for the acute decrease in TSH which occurs after T4 infusion. The data also are consistent with the content that it is nuclear binding of the T3 generated from T4 which initiates the inhibition of TSH release.

Animals↗
PubMed1979

Prolonged intravenous infusion of labelled iodocompounds in the rat: [125I]thyroxine and [125I]tri-iodothyronine metabolism and extrathyroidal conversion of thyroxine to tri-iodothyronine.

Extrathyroidal tissues of the rat were labelled to steady state by prolonged continuous intravenous infusion of 125I-labelled thyroxine (T4) or tri-iodothyronine (T3). Labelled iodocompounds extracted from various tissues were analysed by thin-layer chromatography. Signifficant amounts of labelled T3 were found in all tissues examined after infusion of [125I]T4, confirming that conversion of T4 to T3 occurs in extrathyroidal tissues of the rat. Faecal excretion of labelled T3 after [125I]T4 infusion provided an assessment of the extent of extrathyroidal conversion: about a third of the T4 was metabolized by this pathway. Extrathyroidal conversion was independently estimated to account for about a third of the total production of T3. The site of extrathyroidal conversion was established by comparing the distribution of labelled T3 after the two types of infusion: kidney and liver were both prominent sites of conversion of T4 to T3.

Animals↗
PubMedDate not supplied

[Dissociation between the effects of TSH and dibutyryl cAMP on thyroxine secretion by isolated thyroid cells. Similarity of actions on iodide uptake and thyroxine synthesis (author's transl)].

We have compared the effects of TSH and dibutyryl-cAMP (DBC) on three parameters of iodine metabolism in isolated hog thyroid cells: iodide uptake, thyroxine (T4) synthesis and T4 secretion. As WILSON, we observed a similarity between TSH (60 mU/ml) and DBC (3 mM) actions on iodide uptake and T4 synthesis. But DBC did not reproduce the TSH stimulation of T4 secretion. Since TSH increased T4 secretion in the presence of DBC, the lack of effect of DBC was not due to an alteration of the secretory process by DBC. The present observation might suggest that the stimulatory effect of TSH on T4 secretion by isolated thyroid cells is not mediated by the adenyl cyclase-cAMP system, or could indicate that DBC may not act like cAMP on some target enzyme systems.

Animals↗
PubMed1979

Effects of obesity, total fasting and re-alimentation on L-thyroxine (T4), 3,5,3'-L-triiodothyronine (T3), 3,3',5'-L-triiodothyronine (rT3), thyroxine binding globulin (TBG), cortisol, thyrotrophin, cortisol binding globulin (CBG), transferrin, alpha 2-haptoglobin and complement C'3 in serum.

UNLABELLED: The effects of total fasting for 31 +/- 10 days followed by re-alimentation with an 800 calorie diet on thyroid function, i.e. T4,T3,rT3,RT3U (resin T3 uptake), and TSH, and on TBG levels in serum were studied sequentially in obese hospitalized patients (N=18). Additionally, cortisol, growth hormone, prolactin, parathyrin and free fatty acids were followed as hormonal and metabolic parameters, respectively. Further, CBG, transferrin, alpha 2-haptoglobin and complement C'3 were measured as representatives of other serum proteins. Results before fasting: T4, T3, TBG, cortisol, CBG, alpha 2-haptoglobin and complement C'3 of the obese patients were elevated when compared with healthy normal weight controls, whereas rT3, T4/TBG ratio, T3/TBG ratio, TSH, coritsol/cbg ratio, growth hormone, prolactin, parathyrin and transferrin of the obese group were normal. RT3U and fT4 index were decreased in the obese patients. Results during fasting: Significant decreases were observed during fasting for the following parameters -- T3, TBG, T3/TBG ratio, transferrin, alpha 2-haptoglobin complement C'3. rT3, T4/TBG ratio, RT3U, fT4 index and FFA increased. T4, tsh response to TRH stimulation, cortisol, CBG, cortisol/cbg ratio, parathyrin, growth hormone and prolactin did not change. Results during re-alimentation: T3, TBG, T3/TBG ratio, TSH response to TRH, transferrin, alpha 2-haptoglobin and complement C'3 increased. Conversely, fT3, RT3U, FFA, cortisol and cortisol/cbg ratio decreased whereas the other parameters did not change. CONCLUSIONS: 1) There is no evidence for primary hypothyroidism in obese patients during prolonged fasting and re-alimentation. 2) The rapid decrease of T3 and increase of RT3U after initiation of fasting are not fully explained by the observed slower decreases in TBG. 3) The alterations of T3, rT3 and RT3U resemble in their kinetics the changes in FFA levels. 4) Fasting reduced the levels of only certain serum proteins, interestingly TBG, transferrin, alpha 2-haptoglobin and complement C'3, all of which, except transferrin, are elevated in obesity. 5) The magnitude of the observed decreases does not suggest any clinically relevant deficiencies in serum proteins. 6) Re-alimentation reverses rapidly all observed changes.

Adult↗