Bariatric surgery and 3 year changes in bone mineral density; comparison of four different weight loss modalities (#142)
Bariatric surgery is the most effective intervention for obesity, but little is known about its long term skeletal effects. Some bariatric procedures result in changes in gut-derived, pro-satiety hormones Peptide YY, GLP1 and adiponectin that also affect bone homeostasis. We evaluated the impact of four weight loss interventions, diet (n=13), gastric banding (GB) (n=11), gastric sleeve (GS) (n=21) and Roux-en-Y gastric bypass (RYGB) (n=7), on bone mineral density (BMD) over 36 months. DXA scans were performed at 0, 12, 24 and 36 months along with calciotropic indices, gut hormones and adipokines.
All groups had significant but differing weight loss during first 12 months. Despite weight stability between 12 to 36 months and normal calcium, 25-OH D/ PTH axis, the weight loss modalities resulted in different skeletal responses. RYGB and GS patients experienced continuous total hip BMD loss over 3 years, reaching -14.4% (95%CI -12.2%;-16.7%) for RYGB and -8.7% (95%CI -7.4%;-10.1%) for GS, significantly different from diet group after adjustment for weight loss. RYGB procedure affected multiple skeletal sites causing lumbar spine BMD loss during 1st postoperative year and, over 36 months, forearm BMD loss. No BMD loss was noted for GB and diet groups at any time point. Consistent with bone loss, bone turnover markers (urine uNTx and serum osteocalcin) remained elevated, relative to baseline, up to 3 years post GS and RYGB.
RYGB and GS groups exhibited exaggerated postprandial PYY and adiponectin responses up to 3 years post bariatric surgery. These were inversely associated with TH BMD loss.
The RYGB procedure had a generalised, clinically significant, negative impact on the skeleton. Despite weight stability, RYGB and GS procedures, but not GB and diet, resulted in ongoing TH BMD loss. The rise in postprandial PYY and adiponectin after some bariatric procedures may mediate these skeletal changes.