Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies have provided conflicting evidence as to whether tadpole liver nuclei contain the same number of high affinity binding sites for T4 as they do for T3. Inability to prepare stable tadpole liver nuclei may have contributed to these inconsistencies. Thus, a study was carried out in which the in vivo binding of T4 and T3 by tadpole liver nuclei was reexamined with a greatly improved method for isolating liver nuclei. It was found that the maximum binding capacities of the nuclei for T3 and T4 were not significantly different [0.161 +/- 0.015 (+/- SEM) vs. 0.185 +/- 0.046 pmol/mg DNA]. However, the affinity of the binding sites for T3 was 2-3 times their affinity for T4 (Kd, 1.65 +/- 0.31 vs. 4.32 +/- 0.92 X 10(-12) M). Furthermore, the nuclear binding of [125I]T4 or [125I]T3 was decreased to comparable levels by administration of saturating amounts of T3 and T4 given either before or with the 125I-labeled hormone, indicating that both hormones were competing for the same set of sites. It is suggested that at least some of the previous conflicting findings related to the number of putative thyroid hormone receptors in tadpole liver nuclei are attributable to inadequate methodology which resulted in an overestimation of the maximum binding capacity for T4.
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PMID:Thyroxine and 3,5,3'-triiodothyronine bind to the same putative receptor in hepatic nuclei of Rana catesbeiana tadpoles. 300 95

It is well known that hypothyroidism is frequently associated with impaired GH responses to different stimuli. In the present study we have evaluated GH responses to GH-releasing factor (GRF) in patients with primary hypothyroidism before and during T4 replacement therapy. Fourteen patients (age range 26-60 years) underwent two GRF tests (1 microgram/kg) before and during replacement therapy (150 micrograms/d). Administration of T4 increased peak GH responses to GRF in 9 patients and in the group as a whole (mean +/- SEM, 17.0 +/- 2.8 vs 32.6 +/- 5.7 mU/l, P less than 0.02). When the data are analysed by means of area under the curve (AUC), the GH response to GRF was increased by T4 in 10 patients and in the group as a whole (mean +/- SEM, 51.7 +/- 14.3 vs 101.5 +/- 28.1, P less than 0.02). These data indicate that thyroid hormone replacement therapy enhances the responsiveness of the somatotroph to GRF 1-29 in patients with primary hypothyroidism.
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PMID:Growth hormone responses to GRF 1-29 in patients with primary hypothyroidism before and during replacement therapy with thyroxine. 309 58

The effects of disturbances of thyroid hormone secretion on leg and whole body amino acid and protein metabolism have been investigated in seven patients with untreated thyrotoxicosis and eight patients with untreated hypothyroidism; the results were compared to those obtained in 11 normal control subjects. After treatment, the patients were restudied. Arterio-venous exchanges of tyrosine and 3-methylhistidine across leg tissue in the post-absorptive state were used as indices of net protein balance and myofibrillar protein breakdown, respectively. Whole body protein turnover was measured using stable isotope labelling techniques with 1-[1-13C] leucine. Efflux of tyrosine from leg tissues was six-fold greater in patients with untreated thyrotoxicosis than in normal control subjects (-19.39 +/- 2.21 vs. -4.20 +/- 0.31 nmol 100 g-1 leg tissue min-1, P less than 0.005, mean +/- SEM), but 3-methyl-histidine efflux was not significantly different (-0.11 +/- 0.03 nmol 100 g-1 leg tissue min-1 vs. 0.14 +/- 0.02 nmol 100 g-1 leg tissue min-1). After treatment, when the thyrotoxic patients became euthyroid, tyrosine efflux was normalized (at -4.94 +/- 0.84 nmol 100 g-1 leg tissue min-1) and 3-methylhistidine efflux was unchanged. In hypothyroid patients, neither tyrosine nor 3-methylhistidine effluxes were significantly different from those in normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Skeletal muscle and whole body protein turnover in thyroid disease. 313 Feb 61

To evaluate the effects of thyroid hormones on the concentration of epidermal growth factor (EGF), we determined values for the immunoreactive EGF concentration in the urine (U-irEGF) of newborn infants with congenital hypothyroidism (N = 19), and in urine, saliva and serum of adult patients with hypothyroidism (N = 11) and hyperthyroidism (N = 8). The values were expressed as SD score (SDS), i.e. deviation in SD units from their mean value of healthy subjects of the same age and sex. The SDS of relative U-irEGF (ng/mg creatinine) was lower (P less than 0.01) in newborn infants with congenital hypothyroidism (-0.8 +/- 0.2; mean +/- SEM) than in healthy infants. Their relative U-irEGF correlated with their serum T4 concentrations (r = 0.59, P less than 0.01). The SDS of relative U-irEGF was lower (P less than 0.01) in adult hypothyroid patients (-1.2 +/- 0.5) and higher (P greater than 0.05) in adult hypothyroid patients (0.9 +/- 0.6) than in healthy adult subjects. When subsequently euthyroid, their SDS of relative U-irEGF increased to -0.5 +/- 0.3 (P less than 0.01), and decreased to -0.7 +/- 1.1 (P less than 0.05), respectively. The irEGF concentrations in saliva and serum were not significantly different between the hypothyroid and hyperthyroid patients. Our results indicate that urinary excretion of irEGF in man is dependent on thyroid hormone.
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PMID:Human epidermal growth factor concentrations in urine, but not in saliva and serum, depend on thyroid state. 350 Oct 54

We investigated the serial changes in the plasma levels of anti-thyroglobulin antibody (ATA) by solid-phase enzyme immunoassay, thyroid hormones and blood glucose, since spontaneous occurring lymphocytic thyroiditis (LT) has been found in spontaneously diabetic Bio Breeding/Worcester (BB/W) rat. We also observed the correlation between these levels and histological findings in the thyroid gland. The incidence of diabetes was 0% in 5 week old rats (group A), 70% in 11 week old rats (group B), and 86% in 20 week old rats (group C), while LT was observed in 0% in group A, 20% in group B and 48% in group C. Although the incidence of both increased with age, there was no link between LT and diabetes. Plasma ATA levels were 91.4 +/- 28.5 (OD492 X 1,000, mean +/- SEM) in the control (14 week old Wistar Furth) rats. 49.5 +/- 15.4 in group A, 197.8 +/- 41.5 in group B, and 376.7 +/- 48.7 in group C, again showing a clear increase with age. In group C, the plasma levels of ATA in rats with LT were significantly higher than those without LT. In addition, 6 out of 11 rats without LT had abnormaly high ATA levels. In group C, the plasma levels of free 3,5,3'-triiodothyronine (FT3) and total thyroxine (TT4), and also the FT3/TT4 ratio were significantly lower and the plasma levels of blood glucose were higher than in the other groups. There was no difference between the plasma thyroid hormone levels in rats with LT and those without LT. These studies suggest that LT may occur independently of insulitis, namely diabetes, ATA levels and the incidence of LT increase with age, the site of ATA production may not be confined to the thyroid gland, and the derangement of glucose metabolism may be one of the factors in the decrease in plasma thyroid hormone. The BB/W rat is not only a useful animal model to use in exploring the pathogenesis of human insulin-dependent diabetes mellitus, but also spontaneous autoimmune thyroiditis.
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PMID:Spontaneous autoimmune thyroiditis in Bio Breeding/Worcester (BB/W) rat. 355 49

To appreciate the aldosterone secretion status in panhypopituitarism, the steroid response to stimulation was studied in a homogeneous group of 20 female patients presenting with global hypopituitarism. Specific effects of glucocorticoid and thyroid hormone deficiencies were also assessed by studying the same patients before and after cortisol (F) and cortisol plus thyroid hormone (F + T) substitution. The patients were submitted to two stimulation tests before and after each treatment: the orthostasis test (O-T) and the furosemide test (Furo-T). The results obtained in the 3 situations were compared, each patient serving as her own control. Comparison was also established with the results obtained in healthy women serving as control group. Basal plasma aldosterone levels in the untreated patients were not significantly different from those of the control group (5.43 +/- 0.51 vs 7.16 +/- 0.80 ng/100 ml, mean +/- SEM). They were significantly lower after F (3.91 +/- 0.42) and F + T substitution (3.31 +/- 0.23) than those of untreated patients and controls. Response to both stimulations was blunted in the untreated patients (O-T: 14.10 +/- 2.81; Furo-T: 9.78 +/- 1.35) as compared to the control group (O-T: 26.46 +/- 4.67; Furo-T: 23.96 +/- 3.30). F treatment did not improve the response to either tests, (O-T: 11.42 +/- 2.55; Furo-T: 10.32 +/- 1.23). F + T treatment normalized the orthostasis response (20.83 +/- 3.59) and increased the response to furosemide which remained, however, lower (15.28 +/- 1.83) than in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Aldosterone in panhypopituitarism: dynamic studies and therapeutic effects in Sheehan's syndrome. 375 54

The concentration of FFA in normal human plasma in vivo generally ranges between 0.2 and 0.7 meq/liter; slightly higher concentrations have occasionally been reported in patients who are seriously ill. To determine whether such FFA concentrations may increase the concentration of free T4 in serum, we added increasing amounts of oleic acid to pooled normal human serum (with known FFA content) and measured free T4 by equilibrium dialysis. Total FFA up to 3 meq/liter in normal serum, representing an FFA to albumin molar ratio of about 5:1, had little or no effect on the free T4 concentration, while higher FFA concentrations progressively increased free T4. This same molar ratio of FFA to albumin had to be exceeded to cause a significant increase in the free T4 concentration in diluted serum and in serum from patients with nonthyroid illness. Serum from which more than 95% of the albumin had been removed by chromatography with Affi-Gel blue was much more sensitive to the effects of FFA on free T4. This enhanced sensitivity was reversed by readdition of albumin to the serum, and the addition of albumin to normal serum resulted in diminished effects of FFA on free T4. These results indicate the following: physiological concentrations of FFA do not significantly increase the free T4 concentration in normal human serum; when FFA reach supraphysiological concentrations in serum (in vitro) and the higher affinity FFA-binding sites on albumin become saturated (apparently at an FFA to albumin molar ratio of approximately 5:1), the excess FFA interact with other serum proteins, including thyroid hormone-binding globulin, and thereby increase the free T4 concentration; the concentration of albumin (or other FFA binders) must be considered when evaluating the observed effects of FFA. To explore the relevance of these findings to the hypothesis that FFA may inhibit the binding of T4 to plasma proteins in patients with nonthyroid illness, we measured plasma FFA concentrations in 11 severely ill patients hospitalized in the intensive care unit. We found a mean plasma FFA concentration of 0.45 +/- 0.11 (+/- SEM) mEq/liter and a mean serum albumin concentration of 2.39 +/- 0.29 g/dl in these patients. Their mean plasma FFA to albumin molar ratio was 1.53 +/- 0.41. Since the FFA to albumin molar ratio must exceed about approximately 5:1 before a significant increase in the serum free T4 concentration occurs, these results suggest that FFA do not commonly influence the circulating free T4 concentration in vivo, even in severely ill patients.
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PMID:Effect of free fatty acids on the concentration of free thyroxine in human serum: the role of albumin. 378 24

The regulatory role of thyroid hormones in the synthesis of milk proteins and functional differentiation of the murine mammary gland has been demonstrated. Further, T4 and T3 and their metabolites are found in both rat and human milk. Since the enhanced metabolic demands of mammo- and lactogenesis may result in increased local hormonal requirements, we examined breast tissue from normal (virgin), pregnant, and lactating female rats, as well as postmenopausal human breast tissue for the presence of a thyroid hormone-binding inhibitor (THBI). This substance, which decreases binding of T4 to serum T4-binding globulin, has been described in rat liver, kidney, muscle, and intestine, and in the circulation of patients with nonthyroidal illnesses. THBI activity in the present study was assessed by equilibrium dialysis in whole tissue homogenates; the ether-soluble fraction was also analyzed for THBI activity by RIA. In a range of 0.8-8.0 mg tissue protein, we found lactating rat breast to contain elevated THBI levels when compared to those found in normal, virgin breast tissue. Half-maximum binding inhibition was achieved at 0.15 mg lactating breast tissue protein, vs. 0.23 mg breast tissue protein and 0.35 mg liver protein in homogenates from normal resting animals. Expressed in tissue milligram equivalents, half-maximum binding inhibition of lactating, 18-day pregnant, and normal rat breast tissue was 0.7, 2.6, and 4.8 mgeq, respectively. Thus, the THBI activity of lactating rat breast tissue was more than 3-fold greater than that of the pregnant rat and 7-fold greater than that found in resting breast tissue. Binding inhibition in postmenopausal human breast tissue was comparable to that of rat breast and liver tissue at low protein concentrations, but the maximum inhibition attainable (205 +/- 6%, n = 3) was significantly lower than that achieved by normal rat breast tissue (338 +/- 6%, n = 6; means +/- SEM). The ether-soluble fraction of breast tissue homogenates was also analyzed employing a THBI-RIA. THBI activity, expressed as percent binding inhibition, was elevated in extracts from lactating rat breast tissue in comparison to tissue from pregnant or normal animals at 6.0, 12.5, and 25 mgeq; the largest differences were observed at 25 mgeq tissue: lactating (57.8 +/- 2.3%) vs. pregnant (46.5 +/- 3.1%, P less than 0.01) vs. normal (41.7 +/- 2.3%, P greater than 0.05); n = 3 in all cases.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Thyroid hormone-binding inhibitor in normal, pregnant, and lactating rat and postmenopausal human breast tissue. 392 54

GH secretion is dependent upon thyroid hormone availability. In this study, the GH response to GH-releasing hormone (GHRH) was studied in a group of patients when they were hypothyroid and also when they were euthyroid. Hypothyroidism was associated with a significant reduction in both the peak GH response and the integrated GH secretory response to GHRH compared to those in the euthyroid state [4.7 +/- 1.6 (+/- SEM) vs. 12.2 +/- 3.9 ng/ml (P less than 0.025), and 349 +/- 116 ng vs. 986 +/- 304 ng ml-1 min-1 (P less than 0.025), respectively]. GH responsiveness was impaired within 2 weeks of discontinuation of T3 treatment in athyreotic subjects and was restored within 4 weeks of T4 treatment in one chronically hypothyroid subject. The results imply that a blunted GH response to GHRH in hypothyroidism is attributable to a primary pituitary defect that occurs rapidly and is reversible with attainment of the euthyroid state.
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PMID:Blunted growth hormone (GH) response to GH-releasing hormone in hypothyroidism resolves in the euthyroid state. 392 7

Treatment of myxoedema coma has been associated with a high mortality. The causes of death were analysed in this paper by retrospective study of the records of 11 myxoedema coma patients. The serum thyroxine (T4) and triiodothyronine (T3) levels were estimated retrospectively from the amounts of hormone given to the patients by a two-compartment model. Seven patients died and 4 survived. The patients who died were significantly older (78.9 +/- 2.2 years, mean +/- SEM) than those who survived (66.8 +/- 3.7 years). The initial heart rate was lower in the decreased group, but both groups had increased their heart rate on treatment. The surviving patients showed an increase in body temperature during the first 3 days of treatment, in contrast to the patients who eventually died. The deceased patients had received larger amounts of thyroid hormone and had calculated levels of T3 that were nearly twice as high as those of the surviving patients. Old age and a high serum level of T3 are determinants for the fatal outcome of myxoedema coma. Our analysis underscores the importance of using a cautious replacement regimen in myxoedema coma patients.
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PMID:Treatment of myxoedema coma--factors associated with fatal outcome. 396 12


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