Thyroid Hormone Action on ACTH Secretion

Sánchez‐Franco, Franco; Fernández, Leandro; Fernandez, G.; Cacicedo, Lucinda

doi:10.1055/s-2007-1009285

Cited by 32 publications

(20 citation statements)

References 11 publications

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“…This conclusion is based on measurement of the concentrations of total plasma corticosteroids (7,8), excretion of urinary 17-hydroxysteroids, and assessment of the adrenocortical response to the synthetic adrenocorticotropic hormone (ACTH) 1 -24 (9 -11). None of these measures, however, definitively establishes that thyrotoxicosis is associated with true hyperfunction of the HPA axis.…”

Section: Introductionmentioning

confidence: 99%

Experimentally-induced hyperthyroidism is associated with activation of the rat hypothalamic–pituitary–adrenal axis

et al. 2005

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Objective: Previous studies on the effects of altered thyroid function on the secretion and metabolism of adrenocortical hormones suggest a degree of adrenocortical hyperactivity in hyperthyroidism. We have previously shown that experimentally-induced hyperthyroidism is associated with significant alterations in pituitary -adrenal responsiveness to synthetic ovine corticotropin-releasing hormone (oCRH) that are contingent upon the duration of the altered thyroid function. The purpose of this study was to assess the time-dependent effects of hyperthyroidism on the functional integrity of the hypothalamic -pituitary -adrenal (HPA) axis by in vivo stimulation of the hypothalamic CRH neuron and adrenal cortex. Methods: The functional integrity of the HPA axis was examined in vivo in sham-thyroidectomized male Sprague-Dawley rats given placebo or in thyroidectomized rats given 50 mg of thyroxine every day for 7 or 60 days. Responses to insulin-induced hypoglycemia and IL-1a stimulation were used to assess the hypothalamic CRH neuron. Adrenocortical reserve was assessed in response to low-dose adrenocorticotropic hormone (ACTH), following suppression of the HPA axis with dexamethasone. Adrenal and thymus tissue weight, in addition to basal plasma ACTH, corticosterone and thyroid indices were also determined. Results: Basal plasma corticosterone and corticosterone binding globulin (CBG) concentrations were significantly increased in short-and long-term hyperthyroid rats, and by 60 days, cerebrospinal fluid (CSF) corticosterone levels were significantly increased. Basal plasma ACTH levels were similar to controls. Although plasma ACTH responses to hypoglycemic stress and IL-1a administration in both short-and long-term hyperthyroidism were normal, corticosterone responses to the ACTH release during the administration of these stimuli were significantly increased. The adrenal reserve was significantly elevated in short-term hyperthyroidsim. Long-term hyperthyroidism, however, was associated with a significant reduction in adrenocortical reserve. A significant increase in adrenal weights and a decrease in thymus weights were observed in both short-and long-term hyperthyroidism. Conclusions: The available data confirms that hyperthyroidism is associated with hypercorticosteronemia, although the locus that is principally affected still remains unclear. Despite the sustained hyperactivity of the HPA axis, long-term experimentally-induced hyperthyroidism is associated with diminished adrenal functional reserve. The alterations in HPA function in states of disturbed thyroid function were found to be somewhat more pronounced as the duration of thyroid dysfunction increased.

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Section: Introductionmentioning

confidence: 99%

Experimentally-induced hyperthyroidism is associated with activation of the rat hypothalamic–pituitary–adrenal axis

et al. 2005

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“…The pituitary-adrenal axis is also influenced by the thyroid hormones. In fact, it has been reported that the adrenocortical function is de creased in patients with primary hypothyroidism [13,14] and increased in hyperthyroidism [15] with changes in cortisol clearance rate [14], Furthermore, changes in ACTH secretion have been reported in experimentally in duced thyroid disorders [16], Hypothyroidism decreases the content of several peptides in the anterior pituitary gland and in the central nervous system [17][18][19], Re cently, it has been demonstrated that a deficit in thyroid hormones causes a reduction in galanin (GAL) content in the pituitary and the hypothalamus [20], with disappear ance of GAL immunostaining in fibers within the median eminence and in PVN neurons [21].…”

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confidence: 99%

Response of Hypothalamic Peptide mRNAs to Thyroidectomy

1992

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Using in situ hybridization histochemistry, we have investigated the effect of thyroid hormone on the expression of several peptide mRNAs in the hypothalamic paraventricular nucleus (PVN) of adult male rats. Hypothyroidism was induced by surgical ablation of the thyroid gland. The animals (control sham-operated, thyroidectomized, thyroidectomized + T₄ replaced rats) were studied 28 and 50 days after surgery. Sections of the PVN were hybridized using synthetic oligonucleotide probes complementary to mRNA for thyrotropin-releasing hormone (TRH), corticotropin-releasing hormone (CRH), galanin (GAL), enkephalin (ENK), neurotensin (NT), vasoactive intestinal polypeptide (VIP) and vasopressin (VP). GAL mRNA was also analyzed in the anterior paraventricular, arcuate, and dorsomedial nuclei of the hypothalamus. At the PVN level, a feedback effect of thyroid hormone on TRH synthesis was demonstrated by the TRH mRNA increase in hypothyroidism and by its decrease in hyperthyroidism. Hypothyroidism caused a dramatic decrease in GAL mRNA in parvo- and magnocellular PVN neurons both 28 and 50 days after thyroid ablation, whereas no effect was seen in VP mRNA, the main peptide hormone coexisting with GAL. The T₄ replacement prevented the GAL mRNA impairment. Hypothyroidism did not influence GAL mRNA in the anterior PVN, perifornical area or in the arcuate nucleus, whereas a decrease in GAL mRNA was observed in the dorsomedial nucleus. VIP mRNA, which is undetectable in the PVN of normal animals, was present in several PVN neurons after thyroidectomy. CRH mRNA was decreased after thyroidectomy, whereas the T₄ restitution caused an upregulation. The levels of ENK or NT mRNA were not significantly affected by the thyroid status. The present results show that, in addition to TRH mRNA, other hypothalamic peptide mRNAs are affected by thyroid hormone levels.

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“…Alternatively, the shortened cortisol latency might be due to an activation of nocturnal cortisol secretion. An activation of cortisol by TRH has been described by Sanchez-Franco et al [1989] who demonstrated that experimentally induced hyperthyroidism is associated with the stimulation of ACTH and corticosterone, whereas experimental hypothyroidism showed an inhibition of the hypothalamic-pituitary-adrenal (HPA) axis activity. These results suggest a mutual influence of the two endocrine axes, as previously described by Brabant et al [1987], who found an inhibition of TSH by dexamethasone.…”

Section: Discussionmentioning

confidence: 97%

Effects of Thyrotropin-Releasing Hormone on the Sleep EEG and Nocturnal Hormone Secretion in Male Volunteers

Hemmeter¹,

Rothe²,

Güldner³

et al. 1998

Neuropsychobiology

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Various peptides including corticotropin-releasing hormone (CRH) exert selective effects on sleep structure and noctural secretions of cortisol and growth hormone (GH). In animal studies analeptic effects and sleep disturbances after thyrotropin-releasing hormone (TRH) administration have been observed; studies of endocrine function in depressed patients suggest a pathological activity of CRH and TRH as compared with that in healthy volunteers. As the role of TRH in the regulation of the sleep endocrine pattern in humans has not yet been clarified, we performed a study to examine the effects of pulsatile administration of TRH on the sleep EEG pattern and the nocturnal secretions of cortisol and GH in 7 healthy male subjects. The sleep EEG was recorded from 23.00 to 07.00 h, and blood samples were collected every 20 min from 20.00 to 07.00 h for the analysis of GH and cortisol concentrations during intravenous administration of placebo or 4 × 50 µg TRH at 22.00, 23.00, 24.00, and 01.00 h. In contrast to the well-known effects of CRH on the sleep endocrine pattern, TRH exerts only a weak effect on the sleep EEG which is reflected in a slight decrease in sleep efficiency associated with a trend to wakefulness during the night. Furthermore, after TRH administration, the cortisol rise appeared earlier, and a nonsignificant tendency to an increased secretion of cortisol during the first half of the night was found. The GH secretion did not differ significantly after application of TRH or placebo. The activating, albeit weak, effect of TRH on the sleep EEG and nocturnal cortisol secretion in healthy volunteers confirms and adds to the results previously observed in animals. On the basis of these findings, we surmise that TRH may contribute to the disturbed sleep continuity seen in depressed patients, probably acting as a cofactor of CRH in a synergistic manner.

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Thyroid Hormone Action on ACTH Secretion

Cited by 32 publications

References 11 publications

Experimentally-induced hyperthyroidism is associated with activation of the rat hypothalamic–pituitary–adrenal axis

Experimentally-induced hyperthyroidism is associated with activation of the rat hypothalamic–pituitary–adrenal axis

Response of Hypothalamic Peptide mRNAs to Thyroidectomy

Effects of Thyrotropin-Releasing Hormone on the Sleep EEG and Nocturnal Hormone Secretion in Male Volunteers

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