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.

scholarly journals Effects of Metyrapone Administration on Thyrotropin Secretion in Healthy Subjects–A Clinical Research Center Study*

2000 ◽  
Vol 85 (9) ◽  
pp. 3049-3052
Author(s):  
M. H. Samuels
Keyword(s):  
Healthy Subjects ◽  
Circadian Variation ◽  
Random Order ◽  
Pulse Amplitude ◽  
Serum Cortisol ◽  
Early Morning ◽  
Free T4 ◽  
Tsh Secretion ◽  
Cortisol Levels ◽  
Tsh Levels

Abstract Although pharmacological doses of glucocorticoids suppress TSH secretion, less is known regarding the effects of physiological variations in cortisol levels on TSH. To study this issue, 12 healthy subjects each underwent 2 studies, in random order: 1) each subject received an infusion of saline for 48 h; and 2) each subject received an infusion of saline and oral administration of metyrapone (500 mg every 4 h) for 48 h. Cortisol and TSH levels were measured every 15 min during the final 24 h of each study, and resulting mean hormone levels during the 24-h periods were compared between the two studies. Metyrapone administration reduced serum cortisol levels by 39% between 0800 and 1345 h and by 47% between 0200 and 0745 h, with no significant changes during other time periods. Metyrapone increased daytime (0800–1945 h) mean TSH levels by 35%, with no change in nocturnal (2000–0745 h) TSH levels. This led to equalization of daytime and nocturnal TSH levels and abolition of the usual circadian variation in TSH. TSH pulse frequency was no different between the two studies, whereas daytime TSH pulse amplitude increased 33% during metyrapone administration. There were no changes in TSH responses to TRH, or in serum T3 or free T4 levels, at the end of the studies. These results suggest that the early morning increase in endogenous cortisol levels in healthy subjects causes the daytime decrease in TSH levels. In addition, these results show that very mild changes in cortisol levels within the physiological range are sufficient to affect TSH secretion.

scholarly journals Effects of Variations in Physiological Cortisol Levels on Thyrotropin Secretion in Subjects with Adrenal Insufficiency: A Clinical Research Center Study1

2000 ◽  
Vol 85 (4) ◽  
pp. 1388-1393
Author(s):  
M. H. Samuels
Keyword(s):  
Total Dose ◽  
Adrenal Insufficiency ◽  
Circadian Variation ◽  
Serum Cortisol ◽  
Physiological Study ◽  
Diurnal Pattern ◽  
Baseline Study ◽  
Tsh Secretion ◽  
Cortisol Levels ◽  
Tsh Levels

Although pharmacological doses of glucocorticoids suppress TSH secretion, less is known regarding the effects of physiological variations in cortisol levels on TSH. To study this issue, seven subjects with primary adrenal insufficiency each underwent four studies. In the first study subjects received infusions of saline for 48 h (baseline study). In the second study subjects received infusions of hydrocortisone for 48 h in a pulsatile and diurnal pattern that replicated serum cortisol levels in healthy subjects (physiological study). In most cases, the dose of hydrocortisone was 19 mg/24 h, but this was adjusted as necessary until the resulting serum cortisol levels reproduced those seen in healthy, nonstressed control subjects. In the third study subjects received the same total dose of hydrocortisone as in the physiological study, but with pulses of equal magnitude spaced evenly throughout the time period (constant study). In the fourth study subjects received the same total dose of hydrocortisone, but with the diurnal pattern shifted 12 h from the physiological infusion (reversed study). TSH levels were measured every 15 min during the final 24 h of each study. During the baseline study, the 24-h mean TSH level was 2.87 ± 0.56 mU/L and did not exhibit any diurnal variation. During the physiological study, daytime TSH levels decreased 39% compared to those during the baseline study due to decreased TSH pulse amplitude, and the normal TSH diurnal rhythm was reestablished. The constant and reversed studies did not lead to significant changes in serum TSH levels compared to baseline. These results suggest that the normal circadian variation in endogenous cortisol levels may control TSH secretion, with maximal TSH suppression seen during the time when cortisol levels are highest. However, changing the diurnal pattern of hydrocortisone infusion did not lead to reciprocal changes in TSH levels, and the specific nature of the interactions between cortisol and TSH within the physiological range remains to be fully elucidated.

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.

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

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.

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.

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
Keyword(s):  
Thyroid Hormone ◽  
Testosterone Propionate ◽  
Male Rats ◽  
Thyroxine Treatment ◽  
High Doses ◽  
Serum Tsh ◽  
Tsh Levels

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.

Dysregulation of the Hypothalamic-Pituitary-Adrenal Axis in Postpartum Depression

2007 ◽  
Vol 8 (3) ◽  
pp. 210-222 ◽  
Author(s):  
Sandra N. Jolley ◽  
Shawn Elmore ◽  
Kathryn E. Barnard ◽  
Darcy B. Carr
Keyword(s):  
Postpartum Depression ◽  
Hpa Axis ◽  
Serum Cortisol ◽  
Postpartum Women ◽  
Hypothalamic Pituitary Adrenal ◽  
Clinical Research Center ◽  
Depressed Group ◽  
Longitudinal Study Design ◽  
Cortisol Levels ◽  
Regression Slopes

Postpartum depression (PPD) affects at least 10% to 15% of postpartum women, including more than 600,000 American mothers in 2003 alone. Dramatic changes in the hypothalamic-pituitary-adrenal (HPA) system in the transition from pregnancy to postpartum coupled with research on the psychobiology of depression provided the foundation for this study. The purpose of this study was to compare the reactivity and regulation of the HPA axis components, adrenocorticotropic hormone (ACTH) and cortisol, in depressed and nondepressed postpartum women. A comparative, longitudinal study design was used with 22 normal, healthy, nondepressed pregnant women. Physiologic and postpartum depression data were collected at 6 and 12 weeks postpartum at a university clinical research center. Maximal treadmill exercise stimulated plasma ACTH and serum cortisol levels which were measured before, during, and after 20 min of exercise. Postpartum depression was measured with the Postpartum Depression Screening Scale. Lag within-subject ACTH levels predicting cortisol regression slopes were significantly different between the depressed and nondepressed groups at both 6 and 12 weeks. The depressed group showed no relationship between their ACTH and cortisol levels, with higher ACTH and lower cortisol levels when compared with the nondepressed group. The expected regulated relationship with cortisol levels rising in response to rising ACTH levels was found in the non-depressed group. These findings indicate that the HPA axis was dysregulated in the depressed group, but regulated in the nondepressed group at 6 and 12 weeks postpartum. This pattern of higher ACTH levels to stimulate less cortisol is similar to patterns found in women with early life stresses.

Pharmacokinetics of 3,5,3'-triiodothyroacetic acid and its effects on serum TSH levels

1989 ◽  
Vol 121 (5) ◽  
pp. 651-658 ◽  
Author(s):  
C. Menegay ◽  
C. Juge ◽  
A. G. Burger
Keyword(s):  
Time Course ◽  
Kinetic Studies ◽  
Volume Of Distribution ◽  
Potency Ratio ◽  
Control Serum ◽  
Tsh Secretion ◽  
Dose Response Effect ◽  
Acid Administration ◽  
Serum Tsh ◽  
Tsh Levels

Abstract. 3,5,3'-triiodothyroacetic acid is an effective inhibitor of TSH secretion in central hyperthyroidism. Serum 3,5,3'-triiodothyroacetic acid was measured with an RIA preceded by immunoprecipitation. An anti-3,5,3'-triiodothyroacetic acid antibody was obtained in rabbits, using 3,5,3'-triiodothyroacetic acid coupled to hemocyanin and diazotized benzidine as antigen (crossreactivity with T4, T3, tetraiodothyroacetic acid was 0.2, 1.1, and 5%, respectively). Endogenous 3,5,3'-triiodothyroacetic acid levels could not be detected in 14 euthyroid, 10 hypothyroid and 10 hyperthyroid sera (detection limit 0.055 nmol/l). Kinetic studies were performed in 6 healthy male subjects who received an oral and an iv dose of 1050 μg of 3,5,3'-triiodothyroacetic acid. The serum measurements were analysed according to a non-compartmental method. The half-life of 3,5,3'-triiodothyroacetic acid was 6 h 22 min ± 29 min, the volume of distribution was 114 ± 9 1/70 kg, and the plasma clearance rate was 298 ± 14 1 · (70 kg)−1 · day−1. Highest 3,5,3'-triiodothyroacetic acid levels were measured after 40 min (for T3 2–3 h) and its absorption was 67±6%. The nadir of the mean TSH levels was 0.72 ± 0.09 mU/l 6 h after 3,5,3'-triiodothyroacetic acid administration. However, the time course of serum TSH response did not differ from that obtained after administration of 37.5 μg T3. The dose-response effect for TSH was studied using oral doses of 350, 700, 1400 and 2800 μg 3,5,3'-triiodothyroacetic acid. TSH was measured 9 h after 3,5,3'-triiodothyroacetic acid administration at 17.00 h, and compared with control serum TSH levels obtained at 08.00 h (1.53 ± 0.11) and at 17.00 h the day before the test (1.87 ± 0.11). They were 1.05 ± 0.15 (N = 9, mean ± sem), 0.83 ± 0.08 (N = 24), 0.66 ± 0.06 (N = 24), and 0.43 ± 0.02 mU/l (N = 6), respectively. In conclusion, TSH inhibition by 3,5,3'-triiodothyroacetic acid is similar to T3, with a potency ratio of 1 to 18.

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.

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