Somatostatin immunoneutralization stimulates thyroid function in fowl

1986 ◽  
Vol 110 (1) ◽  
pp. 127-132 ◽  
Author(s):  
S.-K. Lam ◽  
S. Harvey ◽  
T. R. Hall ◽  
G. S. G. Spencer

ABSTRACT The influence of somatostatin on thyroid function has been examined in immature domestic fowl passively immunized with somatostatin antiserum. Plasma thyroxine (T4) and tri-iodothyronine (T3) concentrations were markedly increased within 10 min of antisomatostatin administration and remained raised for at least 5 h. The increases in the T3 and T4 concentrations following somatostatin immunoneutralization were directly related to the volume of antisera administered. The increase in the T3 concentration exceeded the increase in the T4 concentration, resulting in a T3: T4 ratio greater than unity. While the raised T4 concentration began to decline 30 min after antisomatostatin administration, raised T3 concentrations were sustained for at least 2 h, and further increased the plasma T3: T4 ratio. These results demonstrate that somatostatin immunoneutralization stimulates thyroid function in fowl. The magnitude and rapidity of the thyroidal responses to somatostatin immunoneutralization suggests that they occur independently of the hypothalamic-pituitary-thyroid axis. Somatostatin appears to exert a tonic inhibitory control on avian thyroid function, possibly by effects mediated at the thyroid gland to inhibit T4 release and by peripheral effects to suppress the conversion of T4 and T3. J. Endocr. (1986) 110, 127–132

Life ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 426
Author(s):  
Giuseppe Bellastella ◽  
Maria Ida Maiorino ◽  
Lorenzo Scappaticcio ◽  
Annamaria De Bellis ◽  
Silvia Mercadante ◽  
...  

Chronobiology is the scientific discipline which considers biological phenomena in relation to time, which assumes itself biological identity. Many physiological processes are cyclically regulated by intrinsic clocks and many pathological events show a circadian time-related occurrence. Even the pituitary–thyroid axis is under the control of a central clock, and the hormones of the pituitary–thyroid axis exhibit circadian, ultradian and circannual rhythmicity. This review, after describing briefly the essential principles of chronobiology, will be focused on the results of personal experiences and of other studies on this issue, paying particular attention to those regarding the thyroid implications, appearing in the literature as reviews, metanalyses, original and observational studies until 28 February 2021 and acquired from two databases (Scopus and PubMed). The first input to biological rhythms is given by a central clock located in the suprachiasmatic nucleus (SCN), which dictates the timing from its hypothalamic site to satellite clocks that contribute in a hierarchical way to regulate the physiological rhythmicity. Disruption of the rhythmic organization can favor the onset of important disorders, including thyroid diseases. Several studies on the interrelationship between thyroid function and circadian rhythmicity demonstrated that thyroid dysfunctions may affect negatively circadian organization, disrupting TSH rhythm. Conversely, alterations of clock machinery may cause important perturbations at the cellular level, which may favor thyroid dysfunctions and also cancer.


2021 ◽  
Vol 80 (3) ◽  
pp. 567-578 ◽  
Author(s):  
Rosaria Sciarrillo ◽  
Mariana Di Lorenzo ◽  
Salvatore Valiante ◽  
Luigi Rosati ◽  
Maria De Falco

Abstract Different environmental contaminants disturb the thyroid system at many levels. AlkylPhenols (APs), by-products of microbial degradation of AlkylPhenol Polyethoxylates (APEOs), constitute an important class of Endocrine Disrupting Chemicals (EDCs), the two most often used environmental APs being 4-nonylphenol (4-NP) and 4-tert-octylphenol (4-t-OP). The purpose of the present study was to investigate the effects on the thyroid gland of the bioindicator Podarcis siculus of OP alone and in combination with NP. We used radioimmunoassay to determine their effects on plasma 3,3′,5-triiodo-L-thyronine (T3), 3,3′,5,5′-L-thyroxine (T4), thyroid-stimulating hormone (TSH), and thyrotropin-releasing hormone (TRH) levels in adult male lizards. We also investigated the impacts of AP treatments on hepatic 5′ORD (type II) deiodinase and hepatic content of T3 and T4. After OP and OP + NP administration, TRH levels increased, whereas TSH, T3, and T4 levels decreased. Lizards treated with OP and OP + NP had a higher concentration of T3 in the liver and 5′ORD (type II) activity, whereas T4 concentrations were lower than that observed in the control group. Moreover, histological examination showed that the volume of the thyroid follicles became smaller in treated lizards suggesting that that thyroid follicular epithelial cells were not functionally active following treatment. This data collectively suggest a severe interference with hypothalamus–pituitary–thyroid axis and a systemic imbalance of thyroid hormones. Graphic Abstract


2011 ◽  
Vol 57 (2) ◽  
pp. 32-35
Author(s):  
L A Bondarenko ◽  
L Iu Sergienko ◽  
N N Sotnik ◽  
A N Cherevko

The pituitary-thyroid axis of young sexually mature rabbits kept under a 24-hour daylight photoperiod was shown to undergo phase-modulated variations of hormonal activity with its initial increase (during the first month) and subsequent progressive decrease (within 2-5 months after the onset of exposure to light). These changes correlated with the time-dependent fall in the blood T3, T4, and TSH levels. Simultaneously, the animals developed pathological changes in the histological structure of the thyroid gland similar to those in patients with secondary or tertiary hypothyroidism. It is concluded that hormonal and structural changes in the thyroid gland during long-term hypopinealism should be regarded as an experimental model of hypothyroidism of neuroendocrine origin.


Author(s):  
Skand Shekhar ◽  
Raven McGlotten ◽  
Sunyoung Auh ◽  
Kristina I Rother ◽  
Lynnette K Nieman

Abstract Background We do not fully understand how hypercortisolism causes central hypothyroidism or what factors influence recovery of the hypothalamic-pituitary-thyroid axis. We evaluated thyroid function during and after cure of Cushing’s syndrome (CS). Methods We performed a retrospective cohort study of adult patients with CS seen from 2005 – 2018 (cohort 1, c1, n=68) or 1985 – 1994 (cohort 2, c2, n=55) at a clinical research center. Urine (UFC) and diurnal serum cortisol (F: ~8AM and ~midnight (PM)), morning triiodothyronine (T3), free thyroxine (FT4) and thyroid stimulating hormone (TSH) (c1) or hourly TSH from 1500-1900h (day) and 2400-04000h (night) (c2), were measured before and after curative surgery. Results While hypercortisolemic, 53% of c1 had central hypothyroidism (low/low normal fT4 + unelevated TSH). Of those followed long-term, 31% and 44% had initially subnormal FT4 and T3, respectively, which normalized 6—12 months after cure. Hypogonadism was more frequent in hypothyroid (69%) compared to euthyroid (13%) patients. Duration of symptoms, AM and PM F, ACTH, and UFC were inversely related to TSH, FT4 and/or T3 levels (r -0.24 to -0.52, P <0.0001 to 0.02). In c2, the nocturnal surge of TSH (mIU/L) was subnormal before (day 1.00±0.04 vs night 1.08±0.05, p=0.3) and normal at a mean of 8 months after cure (day 1.30±0.14 vs night 2.17±0.27, p=0.01). UFC >1000 μg /day was an independent adverse prognostic marker of time to thyroid hormone recovery. Conclusions Abnormal thyroid function, likely mediated by subnormal nocturnal TSH, is prevalent in Cushing’s syndrome and is reversible after cure.


1977 ◽  
Vol 86 (1) ◽  
pp. 128-139 ◽  
Author(s):  
Isabel Pericás ◽  
Trinidad Jolín

ABSTRACT Studies of pituitary and thyroid function have been carried out in normal (intact) and diabetic Wistar rats. Diabetes was induced by a single streptozotocin injection (7 mg/100 g body weight). The animals were fed a low iodine diet (LID), and received a daily sc injection of either KClO4 (20 mg/100 g body weight) or propylthiouracil (PTU) (1.5 mg/100 g body weight) to induce hypothyroidism. Control groups received the same LID but supplemented with 0.8 μg I/g dry weight. In intact rats goitrogen-treatment induces an increase in thyroid weight and in plasma TSH concentration. However, the plasma TSH response to goitrogen-treatment in diabetics indicates that pituitary TSH secretion increases following a reduction in plasma PBI, but the response is less marked than in controls. The difference in plasma TSH between control and diabetic rats provides an explanation for the findings that diabetes diminishes the thyroid growth response to goitrogen-treatment. Moreover, in intact rats the low pituitary TSH content is a consequence of the increase in pituitary TSH secretion, while in the diabetics the low pituitary TSH content cannot be explained by an increase in TSH secretion. The effect of diabetes on the pituitary-thyroid axis cannot be attributed specifically to poor growth, because the changes in pituitary-thyroid function which are observed in the diabetic groups are not seen in intact rats with a growth rate similar to that of insulin deficient rats. Insulin administration to goitrogen-treated diabetic rats results in 1) an increase in the ability of the thyroid tissue to respond to its trophic hormone, 2) an increase in pituitary TSH secretion in response to the lowering of plasma PBI and, 3) an increase in thyroid growth response to goitrogen-treatment. Results are discussed in relation to the assumption that the lack of adequate insulin levels, or its metabolic defects, diminishes the full response of the thyroid to TSH, and affects the pituitary TSH secretion probably as a consequence of altered hypothalamic control of the pituitary function.


Author(s):  
Timothy M.E. Davis ◽  
Wichai Supanaranond ◽  
Sasithon Pukrittayakamee ◽  
Sanjeev Krishna ◽  
Gillian R. Hart ◽  
...  

1962 ◽  
Vol 41 (6) ◽  
pp. 1703-1707 ◽  
Author(s):  
Ray E. Burger ◽  
F.W. Lorenz ◽  
M.T. Clegg

Endocrinology ◽  
2012 ◽  
Vol 153 (12) ◽  
pp. 6145-6154 ◽  
Author(s):  
Shinjae Chung ◽  
Xiao-Hui Liao ◽  
Caterina Di Cosmo ◽  
Jacqueline Van Sande ◽  
Zhiwei Wang ◽  
...  

Abstract Melanin-concentrating hormone (MCH) is a peptide produced in the hypothalamus and the zona incerta that acts on one receptor, MCH receptor 1 (MCH1R), in rodents. The MCH system has been implicated in the regulation of several centrally directed physiological responses, including the hypothalamus-pituitary-thyroid axis. Yet a possible direct effect of the MCH system on thyroid function has not been explored in detail. We now show that MCH1R mRNA is expressed in thyroid follicular cells and that mice lacking MCH1R [MCH1R-knockout (KO)] exhibit reduced circulating iodothyronine (T4, free T4, T3, and rT3) levels and high TRH and TSH when compared with wild-type (WT) mice. Because the TSH of MCH1R-KO mice displays a normal bioactivity, we hypothesize that their hypothyroidism may be caused by defective thyroid function. Yet expression levels of the genes important for thyroid hormones synthesis or secretion are not different between the MCH1R-KO and WT mice. However, the average thyroid follicle size of the MCH1R-KO mice is larger than that of WT mice and contained more free and total T4 and T3 than the WT glands, suggesting that they are sequestered in the glands. Indeed, when challenged with TSH, the thyroids of MCH1R-KO mice secrete lower amounts of T4. Similarly, secretion of iodothyronines in the plasma upon 125I administration is significantly reduced in MCH1R-KO mice. Therefore, the absence of MCH1R affects thyroid function by disrupting thyroid hormone secretion. To our knowledge, this study is the first to link the activity of the MCH system to the thyroid function.


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