AUGMENTED SECRETION OF TSH IN RESPONSE TO TRH AFTER PRE-TREATMENT WITH DEXAMETHASONE FOR SIX DAYS IN RATS

1976 ◽  
Vol 82 (3) ◽  
pp. 710-714
Author(s):  
Tapio Ranta
Keyword(s):  
Acth Secretion ◽  
Short Term ◽  
Trh Stimulation ◽  
Tsh Secretion ◽  
Pre Treatment ◽  
Dose Levels ◽  
Serum Tsh ◽  
Tsh Levels ◽  
Stimulation Of ◽  
Intact Rats

ABSTRACT Serum TSH and corticosterone concentrations were measured in rats given TRH or exposed to short-term cold, as well as in intact rats, after pretreatment with dexamethasone for six days at two different dose levels (25 and 250 μg/100 g body weight). Both doses increased the secretion of TSH in response to TRH whereas cold-induced TSH secretion was not modified by pre-treatment with dexamethasone. In intact rats serum TSH levels did not differ significantly from controls. In all experiments the steroid blocked ACTH secretion. It was also found that administration of TRH produced a rise in serum corticosterone concentrations. Our results support the view that dexamethasone given for six days facilitates TRH stimulation of the pituitary whilst simultaneously inhibiting the secretion of TRH in response to cold.

Rapid adaptations of serum thyrotrophin, triiodothyronine and reverse triiodothyronine levels to short-term starvation and refeeding

1984 ◽  
Vol 105 (2) ◽  
pp. 194-199 ◽  
Author(s):  
Jean-Noel Hugues ◽  
Albert G. Burger ◽  
A. Eugene Pekary ◽  
Jerome M. Hershman
Keyword(s):  
Serum Cortisol ◽  
Starvation Period ◽  
Short Term ◽  
Mean Values ◽  
Fed State ◽  
Tsh Secretion ◽  
The Mean ◽  
Serum Tsh ◽  
Tsh Levels

Abstract. Nutrition influences thyroid function at the level of TSH secretion, at the level of monodeiodination, and possibly elsewhere. In order to study the effect of starvation on TSH secretion, 8 healthy male volunteers fasted for 30 h and were then refed with 800 kcal. Refeeding was performed at 19.00 h and blood was sampled at 20 min intervals until midnight. Control experiments were performed in the same subjects both when they were normally fed and when the starvation period was prolonged a further 5 h until midnight. Starvation decreased serum TSH levels to below 1 mU/l, and without refeeding the nocturnal peak of the TSH nycthemeral rhythm was abolished. With refeeding serum TSH tended to increase towards midnight and was significantly higher than during starvation. However, the serum TSH levels remained significantly below those at the same time of the day in the absence of a preceding starvation period. Serum T3 levels were significantly lower than in the fed state. The mean values were 1.84 ± 0.03 vs 2.30 ± 0.06 nmol/l (120 ±2 vs 150 ± 4 ng/100 ml, mean ± sem P < 0.01). Refeeding did not result in a measurable change in serum T3 concentration (1.80 ± 0.05 nmol/l; 120 ± 3 ng/100 ml, mean ± sem, n.s.). The contrary was true for rT3 levels which increased in starvation and tended to fall with refeeding, but this decrease was not significant. As glucocorticoids have been implicated in the control of monodeiodination and TSH secretion, serum cortisol levels were also measured. They did not differ during the 3 experimental periods. The results show that short-term starvation and refeeding may be a valuable tool for studying in vivo control of TSH secretion. The results show that short-term starvation and refeeding may be a valuable tool for studying in vivo control of TSH secretion.

NEUROTRANSMITTER CONTROL OF THYROTROPHIN SECRETION IN HYPOTHYROID RATS

1978 ◽  
Vol 89 (1) ◽  
pp. 100-107 ◽  
Author(s):  
P. T. Männistö ◽  
T. Ranta
Keyword(s):  
Dopaminergic System ◽  
Tap Water ◽  
Male Rats ◽  
Noradrenergic System ◽  
High Dose ◽  
Tsh Secretion ◽  
Pre Treatment ◽  
Open Question ◽  
Serum Tsh ◽  
Tsh Levels

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.

INFLUENCE OF PROPYLTHIOURACIL AND THYROXINE ON SYNTHESIS AND SECRETION OF THYROID STIMULATING HORMONE IN THE HYPOTHYROID RAT

1964 ◽  
Vol 46 (1) ◽  
pp. 111-123 ◽  
Author(s):  
John L. Bakke ◽  
Nancy Lawrence
Keyword(s):  
Control Level ◽  
Thyroid Stimulating Hormone ◽  
Synthesis Rate ◽  
Initial Size ◽  
Parallel Increase ◽  
Tsh Secretion ◽  
One Year ◽  
Serum Tsh ◽  
Tsh Levels ◽  
Stimulation Of

ABSTRACT Propylthiouracil (PTU) administration to rats produced a progressive and parallel increase in the serum TSH concentration and the thyroid weight over a one year period, but the pituitary TSH content followed a biphasic curve declining markedly for 4 weeks, returning to the control level in 10 weeks and then continuing to rise until a level 5 times the control was achieved after 32 weeks. Either physiologic replacement doses or toxic doses of thyroxine (DL-T4) caused depression of serum TSH levels, significant as early as one hour after administration, followed by an increased pituitary TSH content to as much as 8 times the starting level after 10-60 hours. Thus, T4 did not appear to directly inhibit TSH synthesis during this interval. The reaction appeared to be independent of the duration of prior PTU administration or the initial size and TSH potency of the pituitary gland or the dose of T4 between 2.5 μg/100 g in one day and 40 μg/100 g daily for 4 days. PTU was not essential to this reaction because it also occurred in radiothyroidectomized rats which never received PTU. This rise in pituitary TSH during the period when TSH secretion was suppressed indicated a net pituitary TSH synthesis of as much as 61 mU/h. These values were compatible with those obtained by indirect calculations and consistent with the temporary persistence of the pre-existing TSH synthesis rate although the possibility of the stimulation of TSH synthesis by the T4 was not excluded.

scholarly journals Thyrotropin Levels during Hydrocortisone Infusions That Mimic Fasting-Induced Cortisol Elevations: A Clinical Research Center Study1

1997 ◽  
Vol 82 (11) ◽  
pp. 3700-3704 ◽  
Author(s):  
M. H. Samuels ◽  
P. A. McDaniel
Keyword(s):  
Healthy Subjects ◽  
Serum Cortisol ◽  
Similar Degree ◽  
Trh Stimulation ◽  
Clinical Research Center ◽  
Tsh Secretion ◽  
Cortisol Levels ◽  
High Doses ◽  
Serum Tsh ◽  
Tsh Levels

Both short term fasting and administration of high doses of glucocorticoids lead to marked suppression of serum TSH levels in healthy subjects. However, it is not known whether the more mild serum cortisol elevations seen during fasting can account for fasting-induced TSH suppression. To study this question, eight healthy subjects each underwent three 2-day studies: 1) baseline (ad libitum diet), 2) fasting (56 h of total caloric deprivation), 3) hydrocortisone (HC) infusions at a dose and pulsatile pattern that reproduced cortisol levels measured during each subject’s fasting study. Subjects required 34–46 mg HC/24 h to achieve these cortisol levels. During each study, blood samples were drawn every 15 min during the final 24 h for serum cortisol and TSH levels. A TRH stimulation test was performed at the end of each study. By design, fasting and HC infusions induced similar mild increases in 24-h serum cortisol levels (32% over baseline), with the most significant increases seen between 1400–0200 h. Fasting decreased 24-h mean and pulsatile TSH levels 65% from baseline, whereas HC infusions decreased mean and pulsatile TSH levels 51% from baseline. Daytime (0800–0200 h) TSH levels were identical in the two studies, whereas nocturnal (0200–0800 h) TSH levels during HC infusions fell midway between baseline and fasting studies. Serum total T3 and TSH responses to TRH were decreased to a similar degree by fasting or HC infusions. These results suggest that mild elevations in endogenous cortisol levels may mediate at least in part fasting-induced changes in TSH secretion and thyroid hormone levels. In addition, these data show that near-physiological doses of HC and resulting changes in serum cortisol levels within the normal range can cause significant decreases in serum TSH levels.

EFFECTS OF INCREASING DOSES OF PYROGLUTAMYL-HISTIDYL-PROLINE AMIDE ON SERUM THYROTROPHIN LEVELS IN NORMAL SUBJECTS

1972 ◽  
Vol 70 (1) ◽  
pp. 196-208 ◽  
Author(s):  
Bengt Karlberg ◽  
Sven Almqvist
Keyword(s):  
Normal Saline ◽  
Standard Dose ◽  
Normal Subjects ◽  
Response Curves ◽  
Clinical Observations ◽  
Trh Stimulation ◽  
Stimulation Tests ◽  
Serial Measurements ◽  
Serum Tsh ◽  
Stimulation Of

ABSTRACT The effects of the administration of normal saline in four normal subjects and the single iv injections of synthetic pyroglutamyl-histidyl-proline amide (TRH) in doses of 6.25, 12.5, 25, 50, 100, 200 and 400 μg in 12 healthy subjects were evaluated by clinical observations and serial measurements from −10 to + 360 minutes of serum TSH, PBI, STH, cholesterol, glucose and insulin. Normal saline and TRH 6.25 μg iv did not change the serum TSH level. The minimum iv dose of TRH increasing serum TSH within 10 minutes was 12.5 μg. Nine of 12 subjects gave maximal increases of serum TSH after TRH 100 μg and all after 200 and 400 μg. The time for the peak response varied with the dose from 15 to 60 minutes. The dose-response curves, average and individual, were complex and not linear. This was interpreted as a varying degree of stimulation of both pituitary synthesis and release of TSH by TRH. PBI changes were measured at 2 h and 6 h. Minimum dose for a significant increase of PBI was 12.5 μg and 6.25 μg of TRH for the respective times. No change in basal STH-levels occurred in 53 of 65 TRH-stimulation tests. Nine of the 12 changes in serum STH occurred in four subjects with varying basal STH-levels. No changes were found in serum cholesterol, glucose or insulin. Our results show that 50 μg of TRH can be used as a standard dose for the single iv stimulation of pituitary release of TSH. TRH stimulated both TSH and STH release in 18% of our tests.

scholarly journals Inhibition of pituitary type 2 deiodinase by reverse triiodothyronine does not alter thyroxine-induced inhibition of thyrotropin secretion in hypothyroid rats

2005 ◽  
Vol 153 (3) ◽  
pp. 429-434 ◽  
Author(s):  
P Cettour-Rose ◽  
T J Visser ◽  
A G Burger ◽  
F Rohner-Jeanrenaud
Keyword(s):  
Specific Inhibitor ◽  
Adult Rats ◽  
Reverse T3 ◽  
Brown Adipose ◽  
Tsh Secretion ◽  
Serum T3 ◽  
Serum T4 ◽  
Serum Tsh ◽  
Tsh Levels

Objectives: Intrapituitary triiodothyronine (T3) production plays a pivotal role in the control of TSH secretion. Its production is increased in the presence of decreased serum thyroxine (T4) concentrations and the enzyme responsible, deiodinase type 2 (D2), is highest in hypothyroidism. In order to document the role of this enzyme in adult rats we developed an experimental model that inhibited this enzyme using the specific inhibitor, reverse T3 (rT3). Methods: Hypothyroidism was induced with propylthiouracil (PTU; 0.025 g/l in drinking water) which in addition blocked deiodinase type 1 (D1) activity, responsible for the rapid clearance of rT3 in vivo. During the last 7 days of the experiment, the hypothyroid rats were injected (s.c.) for 4 days with 0.4 or 0.8 nmol T4 per 100 g body weight (bw) per day. For the last 3 days, the same amount of T4 was infused via s.c. minipumps. In additional groups, 25 nmol rT3/100 g bw per day were added to the 3-day infusion of T4. Results: Infusion of 0.4 nmol T4/100 g bw per day did not affect the high serum TSH levels, 0.8 nmol T4/100 g bw per day decreased them to 57% of the hypothyroid values. The infusions of rT3 inhibited D2 activity in all organs where it was measured: the pituitary, brain cortex and brown adipose tissue (BAT). In the pituitary, the activity was 27%, to less than 15% of the activity in hypothyroidism. Despite that, serum TSH levels did not increase, serum T4 concentrations did not change and the changes in serum T3 were minimal. Conclusions: We conclude that in partly hypothyroid rats, a 3-day inhibition of D2 activity, without concomitant change in serum T4 and minimal changes in serum T3 levels, is not able to upregulate TSH secretion and we postulate that this may be a reflection of absent or only minimal changes in circulating T3 concentrations.

THE INFLUENCE OF METHALLIBURE (ICI 33,828) ON SERUM AND PITUITARY THYROID-STIMULATING HORMONE LEVELS IN THE RAT

1971 ◽  
Vol 49 (4) ◽  
pp. 569-572
Author(s):  
J. R. BOURKE ◽  
S. W. MANLEY ◽  
R. W. HAWKER
Keyword(s):  
Thyroid Stimulating Hormone ◽  
Feedback Mechanism ◽  
Seminal Vesicles ◽  
Endocrine Organs ◽  
System 1 ◽  
Dose Levels ◽  
Higher Doses ◽  
Serum Tsh ◽  
Tsh Levels ◽  
Stimulating Hormone

SUMMARY The effect of methallibure (ICI 33,828), a non-steroidal pituitary inhibitor, on serum and pituitary thyroid-stimulating hormone (TSH) levels has been investigated. A biphasic action of the drug on serum TSH levels was observed, the greatest falls occurring with the lowest doses (2mg/day). Increasing dose and period of administration induced progressive decreases in pituitary TSH content. These results are interpreted in terms of three actions on the thyroid—pituitary system: (1) inhibition of the release of TSH from the pituitary, (2) inhibition of TSH synthesis evident only at higher doses, and (3) a thyroid-blocking action, which is also only observed at the higher dose levels, with consequent pituitary stimulation via the thyroid—pituitary feedback mechanism. Effects upon body weight and weight of endocrine organs are reported, that upon the seminal vesicles being the most marked.

Early effects of aldosterone on Na-K pump in rat cortical collecting tubules

1990 ◽  
Vol 259 (1) ◽  
pp. F40-F45 ◽  
Author(s):  
Y. Fujii ◽  
F. Takemoto ◽  
A. I. Katz
Keyword(s):  
Atpase Activity ◽  
Choline Chloride ◽  
Time Frame ◽  
Short Term ◽  
Rapid Stimulation ◽  
Early Effects ◽  
Collecting Tubules ◽  
Early Interaction ◽  
Stimulation Of ◽  
Intact Rats

Sustained exposure to aldosterone (Aldo) increases the abundance and activity of the Na-K pump in cortical collecting tubules (CCT). However, the onset and mechanism of the early interaction of Aldo with the CCT pump, especially in adrenal-intact animals, are unclear. We evaluated the short-term effects of the hormone on Na-K-adenosinetriphosphatase (ATPase) activity and on ouabain-sensitive 86Rb uptake, a measure of the transporting rate of the pump, in microdissected CCT from adrenal-intact rats. Incubation with Aldo (10(-8) M, 2 h) had no effect on Na-K-ATPase activity (Vmax), whereas it produced at least a twofold increase in 86Rb uptake. This effect was generated by physiological concentrations of the hormone (threshold 10(-10) M; apparent K1/2 approximately 10(-9) M), after a short lag of less than or equal to 30 min. Incubation with Aldo in the presence of amiloride or nystatin or in a Na-free medium (choline chloride) did not prevent the enhanced 86Rb uptake seen after Aldo alone; possible interpretations of these observations are discussed. We conclude that Aldo produces a rapid stimulation of pump function in CCT that precedes its induction of new pump synthesis; the physiological significance of this effect is suggested by its occurrence in tubules from adrenal-intact animals within the time frame and concentration range of the hormone's effects on electrolyte transport.

THE EFFECTS OF PHENYLBUTAZONE ON THYROID FUNCTION

1973 ◽  
Vol 72 (2) ◽  
pp. 257-264 ◽  
Author(s):  
M. O. Abiodun ◽  
R. Bird ◽  
C. W. H. Havard ◽  
N. K. Sood
Keyword(s):  
Thyroid Function ◽  
Significant Rise ◽  
Free Thyroxine ◽  
Continuous Treatment ◽  
Total Serum ◽  
Thyroid Function Tests ◽  
Tsh Secretion ◽  
Total Thyroxine ◽  
Pre Treatment ◽  
Tsh Levels

ABSTRACT It is known that phenylbutazone suppresses the thyroidal uptake of radioactive iodine and the serum level of protein-bound iodine (PBI) during the first week of treatment, with a return to normal values after 2 weeks of continuous treatment. Up till now the initial suppression of thyroid function has been presumed due to inhibition of TSH secretion. In the present study, total serum thyroxine and percentage dialysable thyroxine have been measured and the serum absolute free thyroxine concentration calculated in 12 patients before starting treatment with phenylbutazone orally, after 4 days of treatment and again after 14 days. Serum TSH was assayed in 10 of these patients before, and on the 4th day of treatment. Sera were assayed for TSH after 14 days on the drug in 6 patients. On the 4th day of treatment, the levels of total thyroxine had fallen but the levels of free thyroxine remained unchanged. TSH levels were also unaltered. By the 14th day of treatment, free thyroxine levels had fallen significantly below pre-treatment values but no significant rise in TSH could be demonstrated in the 6 patients studied. At no time was there a fall in TSH levels and we conclude that suppression of some thyroid function tests during the first week of treatment with phenylbutazone is due to direct inhibition of the gland by the drug.

Deficient pulsatile thyrotropin secretion in the low-thyroid-hormone state of severe non-thyroidal illness

1994 ◽  
Vol 130 (2) ◽  
pp. 132-136 ◽  
Author(s):  
Nicola Custro ◽  
Vincenza Scafidi ◽  
Salvatore Gallo ◽  
Alberto Notarbartolo
Keyword(s):  
Thyroid Hormone ◽  
Healthy Subjects ◽  
Normal Subjects ◽  
Healthy Individuals ◽  
Circadian Variations ◽  
Tsh Secretion ◽  
Thyroid Hormone Levels ◽  
Rhythmic Change ◽  
Serum Tsh ◽  
Tsh Levels

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

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