INFLUENCE OF TESTOSTERONE ON THE SECRETION OF THYROTROPHIN IN THE RAT

1965 ◽  
Vol 50 (1) ◽  
pp. 155-160 ◽  
Author(s):  
G. P. van Rees ◽  
E. L. Noach ◽  
J. A. M. J. van Dieten

ABSTRACT Castration of male rats decreases both pituitary and serum TSH-levels. Administration of testosterone propionate increases serum TSH-levels in castrated males, but its effect on pituitary TSH-content appears to be complex: whereas treatment with physiological amounts of testosterone prevents the decrease induced by castration, administration of high doses of testosterone results in low pituitary TSH-contents not unlike those seen in untreated castrated rats. Testosterone administered to thyroxine-maintained thyroidectomized rats had the same effects as mentioned above, but if thyroxine treatment was omitted, no effect of testosterone on pituitary and serum TSH-levels could be observed. It is thought that testosterone interferes with the effect of thyroid hormone on the secretion of TSH.

Author(s):  
Michela Del Prete ◽  
Fabrizio Muratori ◽  
Irene Campi ◽  
Gianleone Di Sacco ◽  
Federico Vignati ◽  
...  

Summary Resistance to thyroid hormone (RTH) is a rare hereditary syndrome with impaired sensitivity to thyroid hormones (TH) and reduced intracellular action of triiodothyronine (T3) caused by genetic variants of TH receptor beta (TRB) or alpha (TRA). RTH type beta (RTHβ) due to dominant negative variants in the TRB gene usually occurs with persistent elevation of circulating free TH, non-suppressed serum TSH levels responding to a thyrotropin-releasing hormone (TRH) test, an absence of typical symptoms of hyperthyroidism and goiter. Here, we present a rare variant in the TRB gene reported for the first time in an Italian patient with generalized RTHβ syndrome. The patient showed elevated TH, with non-suppressed TSH levels and underwent thyroid surgery two different times for multinodular goiter. The genetic test showed a heterozygous mutation in exon 9 of the TRB gene resulting in the replacement of threonine (ACG) with methionine (ATG) at codon 310 (p.M310T). RTHβ syndrome should be considered in patients with elevated TH, non-suppressed TSH levels and goiter. Learning points Resistance to thyroid hormone (RTH) is a rare autosomal dominant hereditary syndrome with impaired tissue responsiveness to thyroid hormones (TH). Diagnosis of RTH is usually based on the clinical finding of discrepant thyroid function tests and confirmed by a genetic test. RTH is a rare condition that must be considered for the management of patients with goiter, elevation of TH and non-suppressed serum TSH levels in order to avoid unnecessary treatments.


2020 ◽  
Author(s):  
Young Jin Kim ◽  
Byoung Kook Kim ◽  
Yong Hyuk Kim

Abstract Background: Various hormones are known to influence the production and secretion of pulmonary surfactant. But the relationship between respiratory distress syndrome (RDS) and thyroid hormone has yet to be clarified. Methods: 126 infants with gestational age between 24 and 34 weeks who were hospitalized at the neonatal ICU of the Wonju Severance Christian Hospital from April 2017 to February 2019 were included in the study. Infants were divided into 3 groups by gestational age – 24 weeks 0 days to 28 weeks 0 days, 28 weeks 0 days to 31 weeks 0 days, and 31 weeks 0 days to 33 weeks 0 days, each with 18, 34, and 74 subjects, respectively. Among the subjects, there were 56 infants with RDS and 70 infants without RDS.Results: The group with lowest gestational age showed T3 and fT4 level that was lower than those of other groups (p<0.05) on the day of birth but there was no difference in the TSH level (p=0.129). T3 and TSH level were lower in the RDS group compared with the control group on the day of birth (p<0.05). Free thyroxine (fT4) level was higher in the control group on the day of birth but without any significant difference. Multiple logistic regression analysis showed that lower serum TSH levels on the day of birth was associated with a higher incidence of RDS (p<0.05).Conclusion: The incidence of RDS was significantly higher in infants with lower serum TSH levels at birth, but there was no significant difference in RDS incidence according to serum thyroid hormone levels.


1981 ◽  
Vol 98 (3) ◽  
pp. 396-401 ◽  
Author(s):  
B. Stringer ◽  
D. Wynford-Thomas ◽  
B. Jasani ◽  
E. D. Williams

Abstract. Adult male rats were fed a goitrogen, aminotriazole, for 74 days at a dose known to suppress thyroid function completely. At the end of this period, these animals along with matched controls were killed in groups of seven at 3 hourly intervals throughout a 24 hour period, and serum TSH, T3, T4 and albumin assayed. No significant circadian rhythms of T3, T4 or albumin were found in either, but a highly significant rhythm of TSH was demonstrated both in controls and goitrogen treated groups, with a diminished relative amplitude in the latter. The results indicate that a significant diurnal rhythm of serum TSH persists in the rat despite long-term blockade of thyroid hormone synthesis and that the existence of this rhythm is therefore independent of the presence of circulating T3 or T4.


1994 ◽  
Vol 130 (2) ◽  
pp. 132-136 ◽  
Author(s):  
Nicola Custro ◽  
Vincenza Scafidi ◽  
Salvatore Gallo ◽  
Alberto Notarbartolo

Custro N, Scafidi V, Gallo S, Notarbartolo A. Deficient pulsatile thyrotropin secretion in the low-thyroid-hormone state of severe non-thyroidal illness. Eur J Endocrinol 1994;130:132–6. ISSN 0804–4643. Twenty-four-hour thyrotropin (TSH) profiles in eight severely ill patients were compared with those of six healthy subjects. The profiles were assessed using the cosinor method to evaluate circadian variations and using the Pulsar algorithm to analyze episodic secretion. In the normal subjects, the typical periodicity of TSH secretion showed a mean level in the rhythm (mesor) of 2.03 mU/l, The amplitude (half the extent of rhythmic change in the cycle) was 0.58 mU/l; the acrophase (the delay from midnight (0 degrees) of the highest level in the rhythm) was −9.9 degrees. In contrast, severely ill patients showed only slight and anticipated elevations of serum TSH levels (mesor 0.93 mU/l, amplitude 0.22 mU/l, acrophase +82.4 degrees). Moreover, whereas the episodic TSH secretion in healthy individuals consisted of 5–8 pulses/24 h, mainly clustered around midnight, only one pulse of reduced amplitude was detected in two of the eight severely ill patients and no pulses in the other six. Since earlier studies have indicated that the loss of TSH pulsatility is associated with the relative insensitivity of the thyrotrophs to low thyroid hormone levels and our analytical procedures have demonstrated that 24 h pulsatile pattern of TSH closely overlapped with baseline TSH secretion, it seems reasonable to assume that low-thyroid-hormone state, deficient pulsatile TSH secretion and altered nyctohemeral TSH periodicity do not coincide by chance, but that there is a causal relationship between such abnormalities in severely ill patients. Nicola Custro, Cattedra di Patologia Medica, Via del Vespro, n.141, 90127 Palermo, Italy


1978 ◽  
Vol 89 (1) ◽  
pp. 100-107 ◽  
Author(s):  
P. T. Männistö ◽  
T. Ranta

ABSTRACT The effect of drugs modifying dopaminergic, noradrenergic and serotonergic systems on the serum TSH levels was studied in the male rats made hypothyroid by giving 10 mg/l of propylthiouracil in tap water for 4 days. Apomorphine (2.5 mg/kg, given once −30 min before sacrifice; or four times −120, 90, 60 and 30 min before sacrifice), bromocryptine (10 and 20 mg/kg, 2 h before sacrifice) and piribedil (50 and 100 mg/kg, 4 h) decreased the serum TSH concentrations. The effect of a single dose of apomorphine (2.5 mg/kg, 30 min before sacrifice) was partially reversed by a pimozide pre-treatment (2.5 mg/kg, 2 h). Clonidine (1 mg/kg but not 0.01 or 0.1 mg/kg, 2 h before sacrifice) further elevated the high TSH levels whereas α-methyl-p-tyrosine (300 mg/kg, 2 h), phenoxybenzamine (50 mg/kg, 2 h) and diethyldithiocarbamate (300 mg/kg, 2 h) significantly decreased TSH secretion. The effect of clonidine (1 mg/kg, 2 h) was partially antagonized by phenoxybenzamine (20 mg/kg, 2 h). A high dose of 5-HTP (300 mg/kg, 2 h) increased serum TSH concentrations whereas p-chlorophenylalanine (100 mg/kg, 2 h) decreased it. When both drugs were given together, the serum TSH levels did not change. L-tryptophan (100–300 mg/kg, 2 h) uniformly decreased the serum TSH concentrations in all experiments. It is concluded that in the hypothyroid rats, the secretion of TSH is inhibited by dopaminergic system, and stimulated by noradrenergic system. The effect of 5-HT pathways remained an open question.


1966 ◽  
Vol 51 (4) ◽  
pp. 619-624 ◽  
Author(s):  
G. P. van Rees

ABSTRACT Levels of thyrotrophin were determined in the anterior pituitary glands and blood sera of thyroidectomized rats after treatment with triiodothyronine or thyroxine for two weeks. The effects of increasing doses of both hormones on pituitary TSH levels appeared to be of a biphasic nature: whereas lower doses caused an increase, higher doses did so to a smaller extent or even caused a decrease, while at the same time progressively depressing the serum TSH levels. The highest pituitary levels found in thyroid hormone treated thyroidectomized rats were similar to those found in untreated intact rats, and equal doses of thyroid hormone were necessary to normalize the increased serum levels as well as the decreased pituitary contents in thyroidectomized animals. These findings are interpreted as indicating that in thyroidectomized rats the rate of release of TSH is depressed by lower doses of triiodothyronine and thyroxine than the rate of synthesis. Triiodothyronine was about three times more active than thyroxine.


1995 ◽  
Vol 132 (6) ◽  
pp. 751-758 ◽  
Author(s):  
Cristiana E Juge-Aubry ◽  
Odette Morin ◽  
Agnés T Pernin ◽  
Hong Liang ◽  
Jacques Philippe ◽  
...  

Juge-Aubry CE, Morin 0, Pernin AT, Liang H, Phillipe J, Burger AG. Long-lasting effects of Triac and thyroxine on the control of thyrotropin and hepatic deiodinase type I. Eur J Endocrinol 1995;132:751–8. The purpose of this study was to investigate the relation between the serum levels of thyroid hormones and their biological effects. For this purpose, hypothyroid rats were studied after stopping treatment with a long-acting thyroid hormone, thyroxine (T4) and a short-acting one, triiodothyroacetic acid (Triac). Based on preliminary experiments with different doses of T4 and Triac, hypothyroid rats (N= 84) received over 6 days' injections of lOnmol Triac or 2 nmol T4/100 g body wt per day. Biological effects of Triac and T4 were measured in the pituitary, liver and kidney up to 8 days after stopping treatment. With Triac, serum thyrotropin (TSH) levels were inhibited completely 6 h after injection, yet after 24 h they were 4.9 ± 1.8 μ/l (hypothyroid 14.5 ± 0.8 μg/l). The rapid changes in serum TSH levels were followed by a more gradual increase in serum TSH levels were followed by a more gradual increase in serum TSH, which was similar to that after T4 injection. Even 8 days after Triac treatment, serum TSH levels did not reach the hypothyroid control levels. Changes in β-TSH mRNA levels also showed a prolonged inhibition after both treatments and a slow return to hypothyroid values, which was not complete 8 days after stopping treatment. A second parameter was hepatic 5′-deiodinase type I (5′D-I), The 6-day treatment with Triac had a markedly stronger effect on 5′D-I enzyme activity and mRNA levels than treatment with T4. Again, the effect disappeared slowly because hepatic activity was still above control levels 8 days after treatment. The mRNA levels of spot 14 also were higher with Triac. However, 4 days after stopping treatment with both hormones, mRNA levels had returned to hypothyroid values. These data suggest that at the pituitary level one can distinguish between rapid and slower effects. For 5′D-I activity, however, the effects are longlasting and there is no apparent difference in the duration of the effects between Triac or T4. They last much longer than the injected hormone. Our results show that even for parameters closely controlled by thyroid hormones, the expression and duration of thyroid hormone effects vary markedly, not only from organ to organ TSH/5′D-I but also within the same organ, depending on the parameters (5′D-I/ spot 14). Cristiana E Juge-Aubry, Thyroid Unit, Hôpital Cantonal Universitaire, 1211 Geneva 14, Switzerland


1979 ◽  
Vol 90 (2) ◽  
pp. 249-258 ◽  
Author(s):  
Pekka Männistö ◽  
Tapio Ranta ◽  
Jouko Tuomisto

ABSTRACT The effect of graded doses of drugs modifying adrenergic activity on basal and cold-stimulated TSH secretion was studied in male rats, ±-Methyl-p-tyrosine (±MPT) (16 h before 30 min cold-exposure), phenoxybenzamine (1 h), Ca-fusarate (1 h) and diethyldithiocarbamate (DDC) (1 and 18 h) dose-dependently depressed the cold-stimulated TSH secretion. The effect of reserpine (24 h) was not significant. Clonidine (1 h), dihydroxyphenylserine (DOPS) (1 h), noradrenaline (NA) (1 h), and l-Dopa (1 h) were also effective in decreasing serum TSH levels, but dopamine (DA) (ad 2 mg/kg, 1 h) had no effect. Basal TSH levels were also decreased by various doses of clonidine, DOPS and NA, given ip 1 h before sacrifice. Clonidine (1 mg/kg), NA (1 mg/kg), DA (2 mg/kg), ±MPT (300 mg/kg), phenoxybenzamine (2 or 20 mg/kg), Ca-fusarate (50 mg/kg) or l-Dopa (200 mg/kg) did not modify the TRH-induced TSH response. These results cannot be explained by assuming only a stimulatory function for the adrenergic system on the secretion of TSH in the rat. The site of the possible inhibitory function of noradrenaline in the control of TSH cannot be deduced from these results, but various possibilities are discussed.


2011 ◽  
Vol 120 (02) ◽  
pp. 121-123 ◽  
Author(s):  
D. Solter ◽  
M. Solter

AbstractDespite some reports, the usefulness of levothyroxine ( LT4) and levotriiodothyronine (LT3) combination therapy in hypothyroidism remains controversial. The objective of this paper is to study a benefit of additional LT3 in athyreotic patients who failed to normalize TSH on LT4 alone even with hyperthyroid serum T4 values.In a survey of 200 athyreotic patients treated between 2006 and 2009, about 7% failed to normalize serum TSH levels following treatment with LT4, though serum T4 values in the hyperthyroid range were achieved. These patients (characterized by serum T4≥160 nmol/L and TSH≥5.0 mIU/L), were additionally treated with 10 μg b. i. d LT3. LT3 and LT4 combination therapy resulted in decreased serum TSH levels into the normal range (12.8 vs. 1.22 mIU/L; p<0.01) and reduced LT4 dose (153.3 vs. 117.5 μg; p<0.01) required for normalization of serum T4 values (170.6 vs. 123.3 nmol/L; p<0.01). Serum T3 values were higher (1.3 vs. 2.26 nmol/L; p<0.01) than those during monotherapy with LT4.Our results indicate a subpopulation of athyreotic patients that could significantly benefit from combined LT4 + LT3 therapy in restoring normal TSH and thyroid hormone patterns. Further research should be undertaken to provide a genetic basis for these findings.


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