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Updated: May 5, 2026

Roux-en-Y Gastric Bypass Operation in Rats
Published on: June 11, 2012
Feeding and bone turnover in gastric bypass
Juan P Valderas1, Oslando Padilla, Sandra Solari
1Departments 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.
Roux-en-Y gastric bypass (RYGB) patients show a preserved, even enhanced, reduction in bone resorption after meals, linked to increased insulin levels. This suggests a bone-protective effect that may offset fasting bone loss.
Area of Science:
- Endocrinology
- Metabolic Surgery
- Bone Metabolism
Background:
- Roux-en-Y gastric bypass (RYGB) surgery is linked to increased bone turnover.
- In healthy individuals, feeding acutely reduces bone resorption, influenced by gut and pancreatic peptides.
Purpose of the Study:
- To investigate bone turnover following meals in patients who have undergone RYGB.
- To compare postprandial bone resorption markers between RYGB patients and a control group.
Main Methods:
- A cross-sectional case-control study involving 15 postmenopausal women post-RYGB and 15 matched controls.
- Measurements included serum parathyroid hormone (PTH), calcium, phosphorus, insulin, carboxy telopeptide (CTX), procollagen type I N-terminal propeptide (P1NP), and glucagon-like peptide 2 (GLP-2) fasting and post-meal.
Main Results:
- Fasting bone turnover markers (CTX, P1NP) were similar or higher in RYGB patients, but postprandial bone resorption (CTX) reduction was more pronounced in RYGB patients.
- RYGB patients exhibited exaggerated postprandial insulin and GLP-2 responses compared to controls.
- A negative correlation was observed between peak insulin levels and CTX reduction.
Conclusions:
- The acute postprandial reduction in bone resorption is maintained and enhanced after RYGB.
- Increased postprandial insulin levels appear to play a role in this bone-protective effect.
- RYGB may possess an intrinsic mechanism to mitigate elevated bone resorption during fasting periods.
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