Effects of neonatal exposure to TRH on development of the pituitary-thyroid axis in rats

1983 ◽  
Vol 104 (2) ◽  
pp. 201-205 ◽  
Author(s):  
Yoshiaki Kawai ◽  
Mizuo Azukizawa ◽  
Nobuyuki Ashida ◽  
Yuichi Kumahara ◽  
Kiyoshi Miyai

Abstract. TRH (10 and 1000 μg/kg body weight) was administered ip daily to neonatal rats from day 0 to 9 after birth (Neo-TRH rats) and their pituitary-thyroid axis was examined on days 4, 10, 21 and 90. The pituitary TSH content in Neo-TRH rats was significantly smaller than in controls on days 4 and 10. The serum TSH levels in Neo-TRH rats were significantly lower than those in controls on days 4 (male group only), 10 and 21 (only 10 μg/kg group). The serum T4 levels in Neo-TRH rats were lower than in controls on day 10. The reduced pituitary TSH content and serum TSH and T4 were restored to control levels on day 90. However, the response of serum TSH to exogenous TRH (10 μg/kg/ip) was blunted in Neo-TRH rats on days 10, 21 and 90. It is concluded that repetitive administration of TRH during the neonatal period suppresses the pituitary-thyroid axis in neonatal life, even after the basal hormone level has been restored to normal.

1978 ◽  
Vol 56 (6) ◽  
pp. 950-955 ◽  
Author(s):  
J. H. Dussault ◽  
P. Walker

The effect of chronic propylthiouracil (PTU) and low iodide diet (LID) on the development of the hypothalamo–pituitary–thyroid axis in the rat has been studied. Pregnant and neonatal rats received 0.05% PTU in their drinking water or LID (distilled water and LID: Teklad Mills, Madison, Wisconsin). Control animals received tap water and Purina rat chow ad libitum. Hypothalamic thyrotropin-releasing hormone (TRH), pituitary and serum thyroid-stimulating hormone (THS), and serum thyroxine (T4) and triiodothyronine (T3) were measured by specific double-antibody radioimmunoassay. Both PTU- and LID-exposed animals had low hypothalamic TRH concentrations at 1 day and a rapid rise to peak levels of 2.4 ± 0.4 pg/μg protein (mean ± SEM) between 12 and 24 days in the PTU animals and 3.2 ± 0.4 pg/μg protein between 12 and 18 days in the LID rats. Hypothalamic TRH concentrations remained relatively stable in the PTU animals, whereas in the LID rats, after a brief but significant decline from 24 to 28 days, hypothalamic TRH concentrations rose to the highest values observed at 57 days (3.9 ± 0.5 pg/μg protein). Both groups of animals had elevated serum TSH levels at 1 day, with higher values seen in the PTU group (p < 0.01), and both showed a rapid rise at 12 days. Thereafter, serum TSH concentrations remained high in the PTU rats but declined to stable, albeit elevated, levels by 24 days (1260 ± 140 ng/ml) in the LID animals. Hypothyroidism was confirmed in the PTU animals by undetectable T4 and reduced T3 concentrations. In the LID rats, serum T4 concentrations rose from undetectable levels at 1 day to stable values by 32 days (2.18 ± 0.13 μg/dl). Serum T3 rose to peak values of 157.0 ± 6.9 ng/dl at 32 days and was elevated at all times after 12 days. These data suggest that chronic exposure to PTU or LID results in a marked derangement of the ontogenetic pattern of the hypothalamo–pituitary–thyroid axis. In addition, neonatal rats exposed to LID appear to respond appropriately by preferential T3 production.


1990 ◽  
Vol 259 (2) ◽  
pp. E162-E169
Author(s):  
M. L. Laakso ◽  
T. Porkka-Heiskanen ◽  
D. Stenberg ◽  
G. Johansson ◽  
P. T. Mannisto

It has been reported that periodicity of lighting plays a role in the regulation of the function of the hypothalamus-anterior pituitary-thyroid axis in the rat. We studied whether other properties of lighting influence the levels of pituitary and serum thyrotropin (TSH) in adult male rats. The animals were reared 7 days under various lighting conditions, then trunk blood and adenohypophyses were collected at different times of the day, and TSH was measured radioimmunologically. In natural lighting conditions the diurnal variation of plasma and pituitary TSH levels was abolished, and the overall levels of plasma TSH were higher and those of pituitary TSH lower than in ordinary laboratory lighting conditions. The intensity of lighting affected the serum TSH levels; daytime serum TSH decreased in the rats under low daytime illuminances and in those under nighttime twilight instead of darkness. Changing the rate of the lighting transition at dawn and dusk had no influence on the TSH patterns. We conclude that, in addition to periodicity, other features of lighting affect the daily secretion patterns of TSH.


Endocrinology ◽  
2011 ◽  
Vol 152 (3) ◽  
pp. 1180-1191 ◽  
Author(s):  
Xiao-Hui Liao ◽  
Caterina Di Cosmo ◽  
Alexandra M. Dumitrescu ◽  
Arturo Hernandez ◽  
Jacqueline Van Sande ◽  
...  

Mice deficient in the thyroid hormone (TH) transporter Mct8 (Mct8KO) have increased 5′-deiodination and impaired TH secretion and excretion. These and other unknown mechanisms result in the low-serum T4, high T3, and low rT3 levels characteristic of Mct8 defects. We investigated to what extent each of the 5′-deiodinases (D1, D2) contributes to the serum TH abnormalities of the Mct8KO by generating mice with all combinations of Mct8 and D1 and/or D2 deficiencies and comparing the resulting eight genotypes. Adding D1 deficiency to that of Mct8 corrected the serum TH abnormalities of Mct8KO mice, normalized brain T3 content, and reduced the impaired expression of TH-responsive genes. In contrast, Mct8D2KO mice maintained the serum TH abnormalities of Mct8KO mice. However, the serum TSH level increased 27-fold, suggesting a severely impaired hypothalamo-pituitary-thyroid axis. The brain of Mct8D2KO manifested a pattern of more severe impairment of TH action than Mct8KO alone. In triple Mct8D1D2KO mice, the markedly increased serum TH levels produced milder brain defect than that of Mct8D2KO at the expense of more severe liver thyrotoxicosis. Additionally, we observed that mice deficient in D2 had an unexplained marked reduction in the thyroid growth response to TSH. Our studies on these eight genotypes provide a unique insight into the complex interplay of the deiodinases in the Mct8 defect and suggest that D1 contributes to the increased serum T3 in Mct8 deficiency, whereas D2 mainly functions locally, converting T4 to T3 to compensate for distinct cellular TH depletion in Mct8KO mice.


1995 ◽  
Vol 133 (1) ◽  
pp. 75-79 ◽  
Author(s):  
Vinay Kamat ◽  
Wendy L Hecht ◽  
Robert T Rubin

Kamat V, Hecht WL, Rubin RT. Influence of meal composition on the postprandial response of the pituitary–thyroid axis. Eur J Endocrinol 1995;133:75–9. ISSN 0804–4643 Ingestion of food can result in an acute decline of serum thyrotropin (TSH) concentrations, but it is not known whether meal composition and/or stomach distension are influential. Normal men and women were given a normocaloric or hypocaloric, isobulk meal at lunch and at dinner in a randomized design. The normocaloric, but not the isobulk, meal resulted in a significant decline in serum TSH at both lunch and dinner; thyroid hormones and cortisol were not affected significantly. These findings suggest that meal composition is influential in the acute postprandial decline of serum TSH in man. A possible mechanism is food-induced elevation of somatostatin and consequent suppression of TSH secretion. Robert T Rubin, Neurosciences Research Center, Allegheny General Hospital, 320 E North Ave. Pittsburgh, PA 15212-4772, USA


2001 ◽  
Vol 169 (1) ◽  
pp. 195-203 ◽  
Author(s):  
J Hassi ◽  
K Sikkila ◽  
A Ruokonen ◽  
J Leppaluoto

In order to evaluate the effects of climatic factors on the secretion of thyroid hormones and TSH in a high latitude population, we have taken serum and urine samples from 20 healthy men from northern Finland (67 degrees -68 degrees N) every 2 months for a period of 14 months. Serum free triiodothyronine (T(3)) levels were lower in February than in August (3.9 vs 4.4 pmol/l, P<0.05) and TSH levels were higher in December than during other months (2.1 vs 1.5-1.7 mU/l, P<0.01). Serum total and free thyroxine (T(4)), total T(3) and reverse T(3) levels and urinary T(4) levels were unchanged. Urinary T(3) levels were significantly higher in winter than in summer. Serum free T(3) correlated highly significantly with the outdoor temperature integrated backwards weekly for 7-56 days (r=0.26 for 1-56 days) from the day when the blood samples were taken. Serum TSH did not show any significant correlation with the thyroid hormones or with the integrated temperature of the previous days, but it did show an inverse and significant correlation (r=-0.31) with the ambient luminosity integrated backwards for 7 days from the day when the blood sample was taken. The gradually increasing correlation between outdoor temperatures and serum free T(3) suggests that the disposal of thyroid hormones is accelerated in winter, leading to low serum free T(3) levels and a high urinary free T(3) excretion. Since there was no correlation between thyroid hormones and serum TSH, the feedback mechanism between TSH and thyroid hormones may not be the only contributing factor, and other factors such as ambient luminosity may at least partly determine serum TSH in these conditions. Also urinary free T(3) appears to be a novel and non-invasive indicator for thyroid physiology.


2018 ◽  
Vol 285 ◽  
pp. 81-86 ◽  
Author(s):  
Marina O. Fernandez ◽  
Nadia S. Bourguignon ◽  
Paula Arocena ◽  
Matías Rosa ◽  
Carlos Libertun ◽  
...  

1987 ◽  
Vol 114 (1) ◽  
pp. 41-46 ◽  
Author(s):  
H. Hohtari ◽  
A. Pakarinen ◽  
A. Kauppila

Abstract. The effects of endurance training and season on the function of the anterior pituitary-thyroid axis were studied in 18 female runners and their 12 controls, and in 13 joggers and their 11 controls in Northern Finland, with a large seasonal difference in environmental factors. The serum concentrations of thyrotropin (TSH), thyroxine (T4), free thyroxine (fT4), triiodothyronine (T3), thyroxine binding globulin (TBG) and oestradiol (E2) were measured during one menstrual cycle in the light training season (autumn) and in the hard training season (spring). The responses of TSH to intravenous TRH stimulation were also measured in the luteal phase of the cycle during the hard training season. Endurance running did not affect the basal or TRH-stimulated serum TSH concentrations, while those of T4 and fT4 in runners were lowered in both seasons and that of T3 in the light training season in relation to control subjects. The serum concentrations of TBG were also significantly lower in runners than their controls in the luteal phase in both seasons. The effect of jogging on thyroid hormones was less pronounced. Serum concentrations of TSH, T4, fT4, T3 and TBG were generally slightly higher in spring than in autumn. Strenuous endurance training seems to have minor changes on the function of the thyroid gland. Depressed T4 levels in runners may rather be due to lowered TBG levels than due to direct effect of training. In spring the function of anterior pituitary-thyroid axis is more active than in autumn.


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.


2008 ◽  
Vol 198 (2) ◽  
pp. 331-337 ◽  
Author(s):  
Isabela Teixeira Bonomo ◽  
Patrícia Cristina Lisboa ◽  
Magna Cottini Fonseca Passos ◽  
Simone Bezerra Alves ◽  
Adelina Martha Reis ◽  
...  

Malnutrition during lactation is associated with hypoprolactinemia and failure in milk production. Adult rats whose mothers were malnourished presented higher body weight and serum tri-iodothyronine (T3). Maternal hypoprolactinemia at the end of lactation caused higher body weight in adult life, suggesting an association between maternal prolactin (PRL) level and programming of the offspring's adult body weight. Here, we studied the consequences of the maternal PRL inhibition at the end of lactation by bromocriptine (BRO) injection, a dopaminergic agonist, upon serum TSH and thyroid hormones, thyroid iodide uptake, liver mitochondrial α-glycerophosphate dehydrogenase (mGPD), liver and pituitary de-iodinase activities (D1 and/or D2), and in vitro post-TRH TSH release in the adult offspring. Wistar lactating rats were divided into BRO – injected with 1 mg/twice a day, daily for the last 3 days of lactation, and C – control, saline-injected with the same frequency. At 180 days of age, the offspring were injected with 125I i.p. and after 2 h, they were killed. Adult animals whose mothers were treated with BRO at the end of lactation presented lower serum TSH (−51%), T3 (−23%), and thyroxine (−21%), lower thyroid 125I uptake (−41%), liver mGPD (−55%), and pituitary D2 (−51%) activities, without changes in the in vitro post-TRH TSH release. We show that maternal PRL suppression at the end of lactation programs a hypometabolic state in adulthood, in part due to a thyroid hypofunction, caused by a central hypothyroidism, probably due to decreased TRH secretion. We suggest that PRL during lactation can regulate the hypothalamus–pituitary–thyroid axis and programs its function.


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