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Estrogen inhibits Dlk1/FA1 production: A potential mechanism for estrogen effects on bone turnover
Author(s) -
Abdallah Basem M,
BayJensen AnneChristine,
Srinivasan Bhuma,
Tabassi Nadine C,
Garnero Patrick,
Delaissé JeanMarie,
Khosla Sundeep,
Kassem Moustapha
Publication year - 2011
Publication title -
journal of bone and mineral research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.882
H-Index - 241
eISSN - 1523-4681
pISSN - 0884-0431
DOI - 10.1002/jbmr.444
Subject(s) - estrogen , mechanism (biology) , bone remodeling , endocrinology , medicine , chemistry , epistemology , philosophy
We have recently identified delta‐like 1/fetal antigen 1 (Dlk1/FA1) as a novel regulator of bone mass that functions to mediate bone loss under estrogen deficiency in mice. In this report, we investigated the effects of estrogen (E) deficiency and E replacement on serum (s) levels of Dlk1/FA1 (s‐Dlk1FA1) and its correlation with bone turnover markers. s‐Dlk1/FA1 and bone turnover markers (serum cross‐linked C‐telopeptide [s‐CTX] and serum osteocalcin) were measured in two cohorts: a group of pre‐ and postmenopausal women ( n = 100) and a group of postmenopausal women, where half had received estrogen‐replacement therapy (ERT, n = 166). s‐Dlk1/FA1 and s‐CTX were elevated in postmenopausal E‐deficient women compared with premenopausal E‐replete women (both p < 0.001). s‐Dlk1/FA1 was correlated with s‐CTX ( r = 0.30, p < 0.01). ERT in postmenopausal women decreased s‐Dlk1/FA1, as well as s‐CTX and s‐osteoclacin (all p < .0001). Changes in s‐Dlk1 were significantly correlated with those observed in s‐CTX ( r = 0.18, p < 0.05) and s‐osteocalcin ( r = 0.28, p < 0.001). In conclusion, s‐Dlk1/FA1 is influenced by E‐deficiency and is correlated with bone turnover. Increased levels of s‐Dlk1/FA1 in postmenopausal women may be a mechanism mediating the effects of estrogen deficiency on bone turnover. © 2011 American Society for Bone and Mineral Research