Erschienen in:
26.11.2018 | Original Contributions
Effects of Biliopancreatic Diversion on Bone Turnover Markers and Association with Hormonal Factors in Patients with Severe Obesity
verfasst von:
Anne-Frédérique Turcotte, Thomas Grenier-Larouche, Roth-Visal Ung, David Simonyan, Anne-Marie Carreau, André C. Carpentier, Fabrice Mac-Way, Laetitia Michou, André Tchernof, Laurent Biertho, Stefane Lebel, Simon Marceau, Claudia Gagnon
Erschienen in:
Obesity Surgery
|
Ausgabe 3/2019
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Abstract
Background
This study evaluated early and medium-term changes in bone turnover markers, and their associations with weight loss, total bone mineral density (BMD), and hormonal changes after biliopancreatic diversion (BPD).
Methods
Ancillary study from a one-year prospective cohort of 16 individuals assessed before, 3 days, 3 and 12 months after BPD. Bone turnover markers (C-terminal telopeptide (CTX), intact osteocalcin (OC), sclerostin, and osteoprotegerin (OPG)) and several hormones were measured at each visit. Total BMD by DXA was assessed at baseline, 3 and 12 months after BPD. Three participants were lost to follow-up.
Results
CTX increased significantly at 3 days (+ 66%), 3 months (+ 219%), and 12 months (+ 295%). OC decreased at 3 days (− 19%) then increased at 3 months (+ 69%) and 12 months (+ 164%). Change in sclerostin was only significant between 3 days and 3 months (+ 13%), while change in OPG was significant between baseline and 3 days (+ 48%) and baseline and 12 months (+ 45%). CTX increase correlated negatively with weight loss at 3 (r = − 0.63, p = 0.009) and 12 months (r = − 0.58, p = 0.039), and total BMD decrease (r = − 0.67, p = 0.033) at 12 months. Change in insulin and adiponectin correlated with changes in bone turnover markers independently of weight loss.
Conclusion
BPD causes an earlier and greater increase in bone resorption over bone formation markers and a decrease in total BMD. Sclerostin did not increase as expected following extensive weight loss. Changes in insulin and adiponectin seem to play a role in the activation of bone remodeling after BPD.