Effects of hypo- and hyperthyroidism on pancreatic TRH-degrading activity and TRH concentrations in developing rat pancreas

1984 ◽  
Vol 106 (2) ◽  
pp. 209-214 ◽  
Author(s):  
Sonia Aratan-Spire ◽  
Bryan Wolf ◽  
Paul Czernichow

Abstract. High concentrations of thyrotrophin-releasing hormone (TRH) in the rat pancreas were detected during the first few days of life decreasing thereafter while pancreatic TRH-degrading activity (TRH-DA) absent at birth appeared on day 14 and increased to reach adult values by day 21. This period of life is also remarkable by the low level of circulating thyroid hormones. Since TRH-degrading activity may be thyroid hormone dependent it was of interest to study the effects of thyroid status fluctuations both on TRH-DA and TRH content during the neonatal period. In this study, hypo- and hyperthyroidism were induced by 6-n-propyl-2-thiouracil (PTU) and triiodothyronine (T3) respectively. Pancreatic TRH-DA and TRH concentrations were measured at different ages from birth until day 29, in treated animals and results compared to control age-matched rats. In hypothyroid rats, pancreatic TRH concentrations remained significantly higher after day 16 while TRH-DA was lower during the whole period studied. Following T3 treatment, pancreatic TRH concentrations decreased significantly from day 3 onwards. However, no significant changes were found for TRH-DA except a two-fold increase on day 28. These results suggest that two different mechanisms may account for thyroid hormones action: 1) a direct effect on pancreatic TRH 2) an inductive saturable effect on TRH-DA. Furthermore a fine tuner modulatory role of TRH-DA on TRH concentrations cannot be excluded.

2009 ◽  
Vol 53 (8) ◽  
pp. 976-982 ◽  
Author(s):  
Simone Magagnin Wajner ◽  
Márcia Santos Wagner ◽  
Ana Luiza Maia

Thyroid hormones are involved in the development and maintenance of virtually all tissues. Although for many years the testis was thought to be a thyroid-hormone unresponsive organ, studies of the last decades have demonstrated that thyroid dysfunction is associated not only with abnormalities in morphology and function of testes, but also with decreased fertility and alterations of sexual activity in men. Nowadays, the participation of triiodothyronine (T3) in the control of Sertoli and Leydig cell proliferation, testicular maturation, and steroidogenesis is widely accepted, as well as the presence of thyroid hormone transporters and receptors in testicular cells throughout the development process and in adulthood. But even with data suggesting that T3 may act directly on these cells to bring about its effects, there is still controversy regarding the impact of thyroid diseases on human spermatogenesis and fertility, which can be in part due to the lack of well-controlled clinical studies. The current review aims at presenting an updated picture of recent clinical data about the role of thyroid hormones in male gonadal function.


2021 ◽  
Vol 19 (2) ◽  
pp. 26-29
Author(s):  
X Lourdes Sandy ◽  

Background: The most common endocrine disorder is hypothyroidism which accounts to 11%. Thyroid hormones have a wide array of functions such as physiological growth and development of skeletal system, maintenance of basal metabolic rate and regulation of various metabolisms, including mineral metabolism. Nowadays due to its direct action on bone turn over, thyroid hormones are considered to have an important role on bone mineral metabolism. Thyroid disorders are important cause for secondary osteoporosis. So the present study was done to know the levels of bone minerals, calcium and phosphorus in hypothyroidism and its relation with thyroid hormone levels. Methods: A case-control study was conducted on 30 hypothyroid patients and 30 euthyroid healthy controls in the age group of 20-60 years. Blood samples were collected from all the study population. Serum total triiodothyronine, total thyroxine and TSH by Enzyme-Linked Immunosorbent Assay, Serum calcium by Arsenazo III method, phosphorous by ammonium molybdate method were estimated. Results: Serum calcium levels in cases was found to significantly reduced when compared to controls (p<0.001). Serum phosphorous levels also showed considerable elevation in cases when compared to controls (p<0.001). There was a significant negative correlation between TSH and serum calcium in cases. Conclusion: The present study indicated the important role of reduced thyroid hormone status on bone mineral metabolism. This study concludes that serum calcium was significantly reduced and phosphorus levels were significantly increased in hypothyroid patients when compared to euthyroid control subjects. So frequent monitoring of serum calcium and phosphorus in hypothyroid patients would reduce the burden of bone pathologies.


1976 ◽  
Vol 71 (1) ◽  
pp. 13-19 ◽  
Author(s):  
N. WHITE ◽  
S. L. JEFFCOATE ◽  
E. C. GRIFFITHS ◽  
K. C. HOOPER

SUMMARY The TRH-degrading activity of rat serum in vitro is five times more potent than that of human serum. In rats, it is significantly reduced in hypothyroidism (thiouracil-induced) and significantly increased in hyperthyroidism (T3 or T4-induced). This suggests a possible role in the regulation of adenohypophysial-thyroid function which is probably, in turn, dependent on thyroid hormone, rather than TSH, levels.


2021 ◽  
Vol 12 ◽  
Author(s):  
Eleonore Fröhlich ◽  
Richard Wahl

Thyroxine and triiodothyronine (T3) are classical thyroid hormones and with relatively well-understood actions. In contrast, the physiological role of thyroid hormone metabolites, also circulating in the blood, is less well characterized. These molecules, namely, reverse triiodothyronine, 3,5-diiodothyronine, 3-iodothyronamine, tetraiodoacetic acid and triiodoacetic acid, mediate both agonistic (thyromimetic) and antagonistic actions additional to the effects of the classical thyroid hormones. Here, we provide an overview of the main factors influencing thyroid hormone action, and then go on to describe the main effects of the metabolites and their potential use in medicine. One section addresses thyroid hormone levels in corona virus disease 19 (COVID-19). It appears that i) the more potently-acting molecules T3 and triiodoacetic acid have shorter half-lives than the less potent antagonists 3-iodothyronamine and tetraiodoacetic acid; ii) reverse T3 and 3,5-diiodothyronine may serve as indicators for metabolic dysregulation and disease, and iii) Nanotetrac may be a promising candidate for treating cancer, and resmetirom and VK2809 for steatohepatitis. Further, the use of L-T3 in the treatment of severely ill COVID-19 patients is critically discussed.


2016 ◽  
Vol 144 (3-4) ◽  
pp. 200-203
Author(s):  
Tijana Lalic ◽  
Biljana Beleslin ◽  
Slavica Savic ◽  
Mirjana Stojkovic ◽  
Jasmina Ciric ◽  
...  

Introduction. In interpreting thyroid hormones results it is preferable to think of interference and changes in concentration of their carrier proteins. Outline of Cases. We present two patients with discrepancy between the results of thyroid function tests and clinical status. The first case presents a 62-year-old patient with a nodular goiter and Hashimoto thyroiditis. Thyroid function test showed low thyroid-stimulating hormone (TSH) and normal to low fT4. By determining thyroid status (?SH, T4, fT4, T3, fT3) in two laboratories, basal and after dilution, as well as thyroxine-binding globulin (TBG), it was concluded that the thyroid hormone levels were normal. The results were influenced by heterophile antibodies leading to a false lower TSH level and suspected secondary hypothyroidism. The second case, a 40-year-old patient, was examined and followed because of the variable size thyroid nodule and initially borderline elevated TSH, after which thyroid status showed low level of total thyroid hormones and normal TSH. Based on additional analysis it was concluded that low T4 and T3 were a result of low TBG. It is a hereditary genetic disorder with no clinical significance. Conclusion. Erroneous diagnosis of thyroid disorders and potentially harmful treatment could be avoided by proving the interference or TBG deficiency whenever there is a discrepancy between the thyroid function results and the clinical picture.


2019 ◽  
Vol 104 (9) ◽  
pp. 3996-4004
Author(s):  
Sofia Galanou ◽  
Giorgos Chouliaras ◽  
Panagiotis Girginoudis ◽  
Chryssanthi Mengreli ◽  
Amalia Sertedaki ◽  
...  

Abstract Context The adrenal gland undergoes substantial remodeling during the neonatal period, an essential developmental process that remains incompletely understood. With respect to control over the remodeling process and, specifically, the role of thyroid hormones (THs), no human studies have been published. The effects of both hypo- and hyperthyroidism have only been evaluated in adults, focusing on the mature adrenal. Recent studies have identified expression of the TH receptor β1 in the mouse adrenal X-zone and have demonstrated that TH administration could alter the postnatal adrenal remodeling process. Objective To address whether THs influence adrenal steroid profiles and adrenal remodeling during the neonatal period. Methods We compared the adrenal steroid profile of a naturally occurring prototype, female neonates with severe congenital hypothyroidism (CH) (n = 22, upon diagnosis of CH), with that of euthyroid neonates (n = 20). Results Significantly higher levels of adrenal steroids (17-OH-progesterone, dehydroepiandrosterone sulfate, Δ4-androstenedione, and testosterone) were measured in neonates with severe CH compared with euthyroid neonates and returned to within normal range after euthyroid state had been established on l-thyroxine replacement therapy, whereas cortisol levels did not differ. TSH values in the CH group were positively correlated with circulating adrenal steroids, whereas free T4 levels were negatively correlated with circulating adrenal steroids. Conclusions The hormonal profile of female neonates with severe CH suggests a more active adrenal fetal zone compared with control subjects. These data indirectly associate THs with the adrenal remodeling and maturation process in humans. Based on our results, we suggest that severe hypothyroidism decelerates the involution of the adrenal fetal zone that normally occurs postnatally.


1982 ◽  
Vol 99 (4) ◽  
pp. 567-572
Author(s):  
Angeles Rodriguez-Pena ◽  
Juan Bernal

Abstract. Two nuclear proteins from rat liver were shown to be dependent on thyroid hormones. These proteins were present in the nucleosol or nucleoplasmic fraction, and were extracted from the nuclei with 0.15 m NaCl at pH8. After thyroidectomy, a 120 000-Mr polypeptide decreased in concentration to levels below 10% of normal control rats and another polypeptide of 81 000-Mr was increased. Treatment with T4 at physiological replacement doses for several days restored the levels of both proteins to normal. A single administration of 50 μg T3 induced a detectable increase of 120K after 14 h, with maximal effects at 48 h after administration. The minimum effective dose of T3 on 120K was 0.5 μg administered for three days. Preliminary observations suggest that the response of 81K to thyroid hormones is much more sensitive than that of 120K. The physiological role of these polypeptides is unknown, but they could be involved in the mode of T3 action at the nuclear level.


2000 ◽  
Vol 352 (3) ◽  
pp. 731-738 ◽  
Author(s):  
Mary C. SUGDEN ◽  
Maria L. LANGDOWN ◽  
Robert A. HARRIS ◽  
Mark J. HOLNESS

Activation of the pyruvate dehydrogenase (PDH) complex (PDHC) promotes glucose disposal, whereas inactivation conserves glucose. The PDH kinases (PDHKs) regulate glucose oxidation through inhibitory phosphorylation of PDHC. The adult rat heart contains three PDHK isoforms PDHK1, PDHK2 and PDHK4. Using Western-blot analysis, with specific antibodies raised against individual recombinant PDHK1, PDHK2 and PDHK4, the present study investigated PDHK isoform expression in the developing rat heart and adulthood. We identified clear differences in the patterns of protein expression of each of these PDHK isoforms during the first 3 weeks of post-natal development, with most marked up-regulation of isoforms PDHK1 and PDHK4. Distinctions between the three cardiac PDHK isoforms were also demonstrated with respect to post-neonatal maturational up-regulation; with greatest up-regulation of PDHK1 and least up-regulation of PDHK4 from the post-neonatal period until maturity. The study also examined the role of thyroid hormone status and lipid supply on PDHK isoform expression. We observed marked selective increases in the amount of PDHK4 protein present relative to total cardiac protein in both hyperthyroidism and high-fat feeding. Overall, our data identify PDHK isoform PDHK1 as being of more potential regulatory importance for glucose oxidation in the adult compared with the neonatal heart, and cardiac PDHK4 as a PDHK isoform whose expression is specifically responsive to changes in lipid supply, suggesting that its up-regulation during early post-natal life may be the perinatal switch to use fatty acids as the energy source. We also identify regulation of pyruvate sensitivity of cardiac PDHK as a physiological variable, a change in which requires factors in addition to a change in lipid supply.


2010 ◽  
Vol 56 (4) ◽  
pp. 443-456 ◽  
Author(s):  
L.I. Nadolnik

The review highlights the effects of acute and chronic stress on thyroid metabolism. Special attention is paid to the influence of stress and the direct effects of glucocorticoids on the thyroid status, the activities of thyrocyte iodine uptake, oxidation and organification as well as peripheral metabolism of thyroid hormones (deposition and transport of thyroid hormones, deiodinase activities in different tissues). The role of stress in the development of thyroid pathology is analysed and charestiristic features of thyroid function alterations during impaired functioning of the pitiutary-adrenal system are established. The mechanisms of the stress-induced impairments in thyroid functions are of interest for further research, taking into consideration serious consequences of thyroid deficiency for the body, even in subclinical thyroid insufficiency.


1974 ◽  
Vol 12 (8) ◽  
pp. 31-32

Thyrotrophin-releasing hormone (TRH - Roche) is a synthetic tripeptide, L-pyroglutamyl-L-histidyl-L-proline-amide, which is identical with the porcine, ovine and human hypothalamic hormone that promotes the secretion of thyrotrophin. Secreted in the hypothalamus, it passes down the capillaries of the pituitary stalk to the anterior pituitary and there causes release of thyrotrophin. Thyroid hormones (triiodo-thyronine (T3) and thyroxine (T4)) interfere with the thyrotrophin (TSH)-releasing action of TRH, so that excess thyroid hormones block TSH release in response to TRH; conversely when thyroid hormone levels are low, increased secretion of TSH occurs. The hypothalamic secretion of TRH is probably directly influenced by the concentration of thyroid hormones in the blood reaching it. In addition TRH promotes the secretion of prolactin from the pituitary. TRH-Roche is marketed in Britain for use in hospitals in diagnostic tests of thyroid and of pituitary-hypothalamic function.


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