Horm Metab Res 1986; 18(4): 268-271
DOI: 10.1055/s-2007-1012291
Clinical

© Georg Thieme Verlag, Stuttgart · New York

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

L. Laurian, Z. Oberman, E. Graf, S. Gilad, E. Hoerer, R. Simantov
  • Departments of Endocrinology, Chemical Pathology and Endocrinological Laboratories, Ichilov Medical Center, Tel Aviv University, Sackler School of Medicine, Weizmann Institute of Science, Tel Aviv, Israel
Further Information

Publication History

1984

1985

Publication Date:
14 March 2008 (online)

Summary

The response of ACTH, β-endorphin and cortisol to calcitonin administration was investigated in 8 subjects with recent fractures of the vertebrae due to postmenopausal or senile osteoporosis (Ost) and in seven normal healthy controls (NO. A significant increase of the three hormones was observed in 13 subjects. The maximum increase was observed between 15 and 60 min.: the cortisol level (μg/100 ml) rose from 14.3 ± 1.9 to 24.8 ± 3.2 (P < 0.05) in Ost and from 7.7±0.6 to 21.7±1.7 (P < 0.001) in NC, the β-endorphin (pmol/l) from 5.8±0.6 and to 21.2±1.3 in OST (P < 0.001) and from 5.9±0.4 to 21.9±4.5 (P <0.01) in NC and the ACTH levels (pg/ml) from 21.3±5.7 to 61.7±3.6 (P < 0.001) in OST and from 30.0±6.2 to 58.8±7.5 (P < 0.05) in NC.

The results indicate a possible role of calcitonin in modulating the anterior pituitary function. It also suggests that the analgesic effect of calcitonin might be mediated by the increase of β-endorphin. The possibility that this analgesic effect of calcitonin is due to its direct binding to the opiate receptors was excluded in the present study by in vitro binding assay.