Calcitonin Induced Increase in ACTH, β-Endorphin and Cortisol Secretion

Laurian, L; Oberman, Z; Graf, Erich Otto; Gilad, S.; Hoerer, E; Simantov, Rabi

doi:10.1055/s-2007-1012291

Cited by 78 publications

(21 citation statements)

References 11 publications

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“…The present data confirm our former observations (Laurian et al, 1986) which showed that calcitonin stimulates 13-endorphin, ACTH and cortisol secretion. Moreover, they show that the stimulatory effect of calcitonin can be inhibited by administration of cyproheptadine.…”

Section: Discussionsupporting

confidence: 93%

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Antiserotonergic inhibition of calcitonin-induced increase of ?-endorphin, ACTH, and cortisol secretion

Laurian

Oberman

Hoerer

et al. 1988

J. Neural Transmission

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In a previous study we observed that calcitonin increases beta-endorphin, ACTH, and cortisol secretion. We assumed that calcitonin might have a modulatory role on the pituitary function. The present study was initiated to clarify whether this effect is due to a direct pituitary stimulation or to an indirect stimulation through CRF (corticotropin releasing factor). Fourteen healthy subjects, aged 30-60 years were investigated. All the subjects received 100 IU Salmon calcitonin Sandoz i.v. at 8 a.m. (time 0). Plasma beta-endorphin, ACTH and cortisol were estimated every 30 min from -30 to 120 min by specific radioimmunoassay. The same parameters were estimated a second time, at the same intervals, when cyproheptadine 8 mg (7 subjects) and 40 mg propranolol (7 subjects) were given per os at -30 min and calcitonin i.v. at time 0. beta-endorphin, ACTH and cortisol levels (Mean +/- SEM) rose significantly after calcitonin (peak value at 30-90 min) from 5.2 +/- 0.7 to 15.1 +/- 2.6 pmol/l; from 43.0 +/- 2.7 to 70.7 +/- 4.1 pg/ml and from 10.6 +/- 1.5 to 19.6 +/- 2.1 micrograms/100 ml respectively (p less than 0.0001 by analysis of variance and covariance and repeated measures). Propranolol 40 mg (per os) administered at time -30 did not alter the response of beta-endorphin, ACTH and cortisol to calcitonin (infused at time 0). Cyproheptadine, the antiserotonergic substance that inhibits the synthesis and release of CRF completely inhibited the stimulatory effect of calcitonin. We conclude that probably calcitonin has a modulatory role on the hypothalamo-pituitary adrenal axis and that it acts at the hypothalamic level probably by stimulating CRF secretion.

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Section: Discussionsupporting

confidence: 93%

“…In a previous study we reported that caldtonin induces a concurrent increase of ACTH, 13-endorphin and cortisol secretion (Laurian et al, 1986).…”

Section: Introductionmentioning

confidence: 88%

Antiserotonergic inhibition of calcitonin-induced increase of ?-endorphin, ACTH, and cortisol secretion

Laurian

Oberman

Hoerer

et al. 1988

J. Neural Transmission

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“…Besides the hypocalcemic effect of CT, it is well established that CT administration shows regulatory effects on a variety of hormone secretion. Secretion of gastrin [6], insulin [3], GH [16], TSH [15], prolactin [20], and prostaglandin [4] were suppressed by the preinfusion of CT. On the other hand, hormone secretions were stimulated by CT infusion in the following hormones, such as ACTH [14], somatostatin [5,10,17], and beta-endorphin [14] secretions. Auto-regulation of CT secretion has been suggested as a feedback mechanism by some researchers using porcine thyroid slices [1,21].…”

Section: Introductionmentioning

confidence: 99%

Exogenous Calcitonin Suppresses Growth Fraction of Thyroid C Cells

Mori

Nakamura

Iteya

et al. 2003

Acta Histochem. Cytochem

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Calcitonin (CT) is a peptide hormone synthesized and secreted by the parafollicular (C) cells of the thyroid. Little is known about the mechanisms controlling proliferation of C cells by other humoral factors including CT, and there is no report that CT suppresses C cell proliferation. The effects of short-term administration of CT on C cell growth fraction were analyzed using BrdU and CT double immunohistochemical method in the rat thyroid. Continuous administration of 0.4 IU/kg and 40 IU/kg synthetic salmon CT for 14 days induced dosedependent suppression of BrdU labeling number of C cells without decrease of C cell to the total thyroid follicular cell ratio. These results suggest that exogenous CT may induce negative feedback to C cell proliferation in the thyroid.

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“…Firstly, it inhibits cyclooxygenase, thus lessening the production of prostaglandins and thromboxane A2 in guinea pig lung (18) and humans (19); however, other studies have found opposite results (20). Secondly, it has been shown to increase ACTH, ß-endorphin and cortisol serum levels (21), indicating a possible role in modulation of the anterior pituitary function, but this is challenged in other studies (22). Thirdly, specific binding sites for salmon calcitonin have been found in the brain of animals (23,24) and humans (25), suggesting a central intrinsic analgesic effect; supported by the successful use of calcitonin as a subarachnoid or epidural injection in humans (26).…”

Section: Discussionmentioning

confidence: 99%

Analgesic activity of high-dose intravenous calcitonin in cancer patients with bone metastases

Tsavaris

Kopterides²,

Kosmas³

et al. 2006

Oncol Rep

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Abstract. We undertook a prospective, nonrandomized study with the objective to evaluate the efficacy of salmon calcitonin (sCT) in controlling pain secondary to bone metastases. Our study population consisted of 45 cancer patients with bone metastases (26 men) with a mean age of 64 years (range, 48-70) who had completed chemotherapy, hormonal therapy and radiation therapy at least 30 days prior to enrollment in the study, and had intractable pain despite the use of common analgesics (acetaminophen, nonsteroidal anti-inflammatory agents, opioids) and bisphosphonates. The study medication was a 300-IU dose of sCT administered intravenously daily for 5 consecutive days and repeated every two weeks until no response was noticeable. The analgesic efficacy of sCT was evaluated by means of Huskisson's visual analogue scale and Keele's pain scale; the daily consumption of analgesic drugs and performance status were also monitored. None of the patients managed to completely discontinue the use of other analgesics, but 5 patients (11% of the total number) had an analgesic response that lasted 4 weeks and less than 5% of the patients continued to respond for 6 weeks. No significant side effects were observed. Our data show that intravenous calcitonin administered in a relatively high dose has a very limited therapeutic potential as an adjuvant analgesic for a short period of time in selected cancer patients with bone metastases.

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Calcitonin Induced Increase in ACTH, β-Endorphin and Cortisol Secretion

Cited by 78 publications

References 11 publications

Antiserotonergic inhibition of calcitonin-induced increase of ?-endorphin, ACTH, and cortisol secretion

Antiserotonergic inhibition of calcitonin-induced increase of ?-endorphin, ACTH, and cortisol secretion

Exogenous Calcitonin Suppresses Growth Fraction of Thyroid C Cells

Analgesic activity of high-dose intravenous calcitonin in cancer patients with bone metastases

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