Effects of Biliopancreatic Diversion on Bone Turnover Markers and Association with Hormonal Factors in Patients with Severe Obesity
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).
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.
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.
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.
KeywordsBiochemical markers of bone turnover Bariatric surgery Biliopancreatic diversion Bone mineral density Hormones
The Canadian Institutes of Health Research (MOP 97947), Diabetes Canada and CHU de Québec Foundation provided funding for this research.
Compliance with Ethical Standards
Conflict of Interest
AMC is the recipient of Fonds de recherche du Québec-Santé (FRQ-S) and Diabetes Canada scholarships. ACC is the recipient of the GSK Chair in Diabetes of Université de Sherbrooke. LM reports non-financial support from Roche Diagnostics Canada, personal fees from Amgen, personal fees from Eli Lilly, personal fees from Abbvie, personal fees from Bristol-Myers Squibb, personal fees from Novartis, outside the submitted work. AT and LB receive funding from Johnson Johnson Medical Companies and Medtronic for research studies on bariatric surgery. CG is a clinical research scholar of the FRQ-S and the recipient of a Diabetes Canada New Investigator Award. She received research funding from Technologies Khlôros, and speaker honoraria from Amgen, Eli Lilly, and Janssen. All other authors report no conflicts of interest.
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