NOCTURNAL RISE IN MARKERS OF BONE-RESORPTION IS NOT ABOLISHED BY BEDTIME CALCIUM OR CALCITONIN

Citation
S. Sairanen et al., NOCTURNAL RISE IN MARKERS OF BONE-RESORPTION IS NOT ABOLISHED BY BEDTIME CALCIUM OR CALCITONIN, Calcified tissue international, 55(5), 1994, pp. 349-352
Citations number
17
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
0171967X
Volume
55
Issue
5
Year of publication
1994
Pages
349 - 352
Database
ISI
SICI code
0171-967X(1994)55:5<349:NRIMOB>2.0.ZU;2-T
Abstract
As assessed by urine pyridinium cross-links, bone resorption increases at night. This has been ascribed to either the nocturnal rise of seru m parathyroid hormone (PTH) or immobilization. ICTP is the carboxyterm inal telopeptide region of type I collagen in bone, cross-linked via p yridinium cross-links and liberated during the degradation of type I c ollagen. To study whether the nocturnal rise in bone resorption is see n also in serum type I collagen carboxyterminal telopeptide (ICTP) and whether this rise is abolished by bedtime calcium or calcitonin, nine healthy postmenopausal women participated in three 24 hour sessions. At 2200 hours, either 1 g of oral calcium or 200 IU of intranasal calc itonin or no treatment (control session) were given. The participants were recumbent from 2200 hours to 0600 hours. Like urinary pyridinolin es, serum ICTP showed a clearcut nocturnal rise during the control ses sion, increasing from 3.7 +/- 0.3 mu g/liter (mean +/- SE) at 2000 hou rs to 4.9 +/- 0.4 mu g/liter at 0600 hours (P < 0.001). Administration of calcium did not affect either serum ICTP or urinary pyridinolines, although it decreased serum intact PTH by 18% (P < 0.001) as assessed by areas under curve (AUC) after 2200 hours. Serum ICTP and urinary p yridinolines remained unchanged also after administration of calcitoni n which increased the AUC for serum intact PTH by 9% (P < 0.05). In co nclusion, serum ICTP follows a circadian rhythm in healthy postmenopau sal women. The nocturnal rise in markers of bone resorption is not due to PTH, and its dependency on the function of osteoclasts is open to question.