title: Cortical and trabecular deterioration in mouse models of Roux-en-Y gastric bypass.
abstract: Roux-en-Y gastric bypass (RYGB) is a profoundly effective treatment for severe obesity, but results in significant bone loss in patients. Developing a murine model that recapitulates this skeletal phenotype will provide a robust tool with which to study the physiologic mechanisms of this bone loss. We studied adult male C57BL/6J mice who underwent either RYGB or sham operation. Twelve weeks after surgery, we characterized biochemical bone markers (parathyroid hormone, PTH; C-telopeptide, CTX; and type 1 procollagen, P1NP) and bone microarchitectural parameters as measured by microcomputed tomography. RYGB-treated mice had significant trabecular and cortical bone deficits compared with sham-operated controls. Although adjustment for final body weight eliminated observed cortical differences, the trabecular bone volume fraction remained significantly lower in RYGB mice even after weight adjustment. PTH levels were similar between groups, but RYGB mice had significantly higher indices of bone turnover than sham controls. These data demonstrate that murine models of RYGB recapitulate patterns of bone loss and turnover that have been observed in human clinical studies. Future studies that exploit this murine model will help delineate the alterations in bone metabolism and mechanisms of bone loss after RYGB.
authors.affiliation: Endocrine Unit, Massachusetts General Hospital, USA.
authors.forename: Elaine W
authors.initials: EW
authors.lastname: Yu
authors.affiliation: Obesity, Metabolism, and Nutrition Institute and Gastrointestinal Unit, Massachusetts General Hospital, USA.
authors.forename: Jill S
authors.initials: JS
authors.lastname: Carmody
authors.affiliation: Endocrine Unit, Massachusetts General Hospital, USA; Center for Advanced Orthopedic Studies, Beth Israel Deaconess Medical Center, USA.
authors.forename: Daniel J
authors.initials: DJ
authors.lastname: Brooks
authors.affiliation: Obesity, Metabolism, and Nutrition Institute and Gastrointestinal Unit, Massachusetts General Hospital, USA.
authors.forename: Scott
authors.initials: S
authors.lastname: LaJoie
authors.affiliation: Obesity, Metabolism, and Nutrition Institute and Gastrointestinal Unit, Massachusetts General Hospital, USA.
authors.forename: Lee M
authors.initials: LM
authors.lastname: Kaplan
authors.affiliation: Endocrine Unit, Massachusetts General Hospital, USA; Center for Advanced Orthopedic Studies, Beth Israel Deaconess Medical Center, USA.
authors.forename: Mary L
authors.initials: ML
authors.lastname: Bouxsein
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D001835:Body Weight; D016723:Bone Remodeling; D000071556:Cancellous Bone / Q000378:metabolism / Q000473:pathology*; D000071538:Cortical Bone / Q000378:metabolism / Q000473:pathology*; D015390:Gastric Bypass; D008297:Male; D008810:Mice, Inbred C57BL; D023421:Models, Animal; D010281:Parathyroid Hormone / Q000378:metabolism
chemical_list: D015415:Biomarkers; D010281:Parathyroid Hormone
keywords: Bariatric surgery; Bone loss; Bone microarchitecture; Gastric bypass; Mouse models; Obesity; Weight loss