title: Feeding and bone turnover in gastric bypass.
abstract: BACKGROUND
  Roux-en-Y gastric bypass (RYGB) is associated with high bone turnover. In healthy subjects, feeding causes acute reduction of bone resorption, which is regulated by several intestinal and pancreatic peptides.
  
  
  OBJECTIVE
  Our objective was to assess bone turnover after feeding in patients with RYGB.
  
  
  METHODS
  This was a cross-sectional case-control study at a university hospital.
  
  
  METHODS
  Fifteen postmenopausal women who underwent RYGB 7.4 ± 4.1 years previously were matched by age and body mass index with 15 nonoperated women (controls).
  
  
  RESULTS
  Serum PTH, calcium, phosphorus, insulin, carboxy telopeptide (CTX), procollagen type I N-terminal propeptide (P1NP), and glucagon-like peptide 2 (GLP-2) were measured while fasting and after a standard meal (SM).
  
  
  RESULTS
  The fasting calcium, phosphorus, and PTH were similar in both groups and exhibited similar decreases after an SM. The fasting CTX level was higher in the RYGB than in the control group (0.589 ± 0.18 vs 0.382 ± 0.11 ng/mL; P < .05) and fell to a nadir of 42.2% of the basal value in the RYGB and 53.9% in controls (P < .05). The fasting and postprandial P1NP levels were similar in both groups and fell to a nadir of 85.8% in the RYGB and 89.3% in controls. Insulin and GLP-2 levels were similar during fasting in both groups. RYGB patients had exaggerated postprandial insulin and GLP-2 response compared with the controls with the insulin and GLP-2 area under the curve being significantly higher in the RYGB group. There was a significant negative correlation between the peak of insulin levels and the CTX changes.
  
  
  CONCLUSIONS
  The acute reduction in bone resorption after feeding is preserved in RYGB and is even higher than in nonoperated subjects. This phenomenon is related to the increase of postprandial levels of insulin. These findings suggest a bone-protecting mechanism in RYGB that may counteract the elevated bone resorption that occurs during fasting.
authors.affiliation: Departments of Nutrition, Diabetes, and Metabolism (J.P.V., M.E.), Public Health (O.P.), Clinical Laboratories (S.S.), and Endocrinology (G.G.), School of Medicine, Pontificia Universidad Católica de Chile, 6510260 Santiago, Chile.
authors.forename: Juan P
authors.initials: JP
authors.lastname: Valderas
authors.forename: Oslando
authors.initials: O
authors.lastname: Padilla
authors.forename: Sandra
authors.initials: S
authors.lastname: Solari
authors.forename: Manuel
authors.initials: M
authors.lastname: Escalona
authors.forename: Gilberto
authors.initials: G
authors.lastname: González
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose; D016723:Bone Remodeling / Q000502:physiology*; D002118:Calcium / Q000097:blood; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D005260:Female; D015390:Gastric Bypass; D053767:Glucagon-Like Peptide 2 / Q000097:blood; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance / Q000502:physiology; D008875:Middle Aged; D009767:Obesity, Morbid / Q000097:blood / Q000601:surgery*; D010281:Parathyroid Hormone / Q000097:blood; D010758:Phosphorus / Q000097:blood; D019518:Postprandial Period
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D053767:Glucagon-Like Peptide 2; D007328:Insulin; D010281:Parathyroid Hormone; D010758:Phosphorus; D002118:Calcium