Physical activity in relation to serum sclerostin, insulin-like growth factor-1, and bone turnover markers in healthy premenopausal women: a cross-sectional and a longitudinal study.

J Clin Endocrinol Metab

Center of EXcellence for Osteoporosis Research, Department of Clinical Biochemistry, Faculty of Medicine and King Abdulaziz University Hospital, King Abdulaziz University, P.O. Box 20724, Jeddah 21465, Saudi Arabia.

Published: October 2012

Context: There is limited information on the effects of mechanical loading caused by physical activity (PA) on sclerostin, IGF-I, and bone turnover markers (BTM).

Objective: The objective of the investigation was to study the relationships between serum sclerostin, serum-IGF-I (s-IGF-I), BTM, and the PA level in premenopausal women and to discern how 8 wk of PA training (PAT) affects the serum levels of sclerostin, IGF-I, and BTM.

Design: This was a cross-sectional study with a subgroup followed up longitudinally.

Settings And Subjects: A total of 1235 randomly selected premenopausal women were cross-sectionally studied. We also followed up 58 of these women longitudinally during an 8-wk course of PAT (4 d/wk) and compared them with 62 controls. All women were medically examined, and bone mineral density (BMD) and serum levels of sclerostin, s-IGF-I, and BTM were determined.

Results: Women with PA of greater than 120 min/wk showed significantly lower serum sclerostin (by 36.8%) but higher s-IGF-I (by 107%) levels than sedentary controls. Bone formation markers were also higher in the PA greater than 120 min/wk group compared with the sedentary controls. In the longitudinal study, the 8-wk PAT program led to a decrease in serum sclerostin (by 33.9%, P<0.0001) but increases in the serum levels of the bone-formation markers and IGF-I (s-IGF-I by 74.2%, P<0.0001).

Conclusions: This study demonstrates that even minor changes in PA are associated with effects on serum levels of sclerostin, IGF-I, and BTM and suggests that sclerostin could be a link between mechanical loading and disuse osteoporosis in humans.

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http://dx.doi.org/10.1210/jc.2011-3361DOI Listing

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