title: Increased bone resorption and impaired bone microarchitecture in short-term and extended high-fat diet-induced obesity.
abstract: Although obesity traditionally has been considered a condition of low risk for osteoporosis, this classic view has recently been questioned. The aim of this study was to assess bone microarchitecture and turnover in a mouse model of high-fat diet-induced obesity. Seven-week-old male C57BL/6J mice (n = 18) were randomized into 3 diet groups. One third (n = 6) received a low-fat diet for 24 weeks, one third was kept on an extended high-fat diet (eHF), and the remaining was switched from low-fat to high-fat chow 3 weeks before sacrifice (sHF). Serum levels of insulin, leptin, adiponectin, osteocalcin, and cross-linked telopeptides of type I collagen (CTX) were measured. In addition, bone microarchitecture was analyzed by micro-computed tomography; and lumbar spine bone density was assessed by dual-energy x-ray absorptiometry. The CTX, body weight, insulin, and leptin were significantly elevated in obese animals (sHF: +48%, +24%, +265%, and +102%; eHF: +43%, +52%, +761%, and +292%). The CTX, body weight, insulin, and leptin showed a negative correlation with bone density and bone volume. Interestingly, short-term high-fat chow caused similar bone loss as extended high-fat feeding. Bone volume was decreased by 12% in sHF and 19% in eHF. Bone mineral density was 25% (sHF) and 27% (eHF) lower when compared with control mice on low-fat diet. As assessed by the structure model index, bone microarchitecture changed from plate- to rod-like appearance upon high-fat challenge. Trabecular and cortical thickness remained unaffected. Short-term and extended high-fat diet-induced obesity caused significant bone loss in male C57BL/6J mice mainly because of resorptive changes in trabecular architecture.
authors.affiliation: Division of Cellular and Molecular Pathophysiology, Department of Pathophysiology, Center of Physiology, Pathophysiology and Immunology, Medical University Vienna, A-1090 Vienna, Austria.
authors.forename: Janina M
authors.initials: JM
authors.lastname: Patsch
authors.forename: Florian W
authors.initials: FW
authors.lastname: Kiefer
authors.forename: Peter
authors.initials: P
authors.lastname: Varga
authors.forename: Pamela
authors.initials: P
authors.lastname: Pail
authors.forename: Martina
authors.initials: M
authors.lastname: Rauner
authors.forename: Daniela
authors.initials: D
authors.lastname: Stupphann
authors.forename: Heinrich
authors.initials: H
authors.lastname: Resch
authors.forename: Doris
authors.initials: D
authors.lastname: Moser
authors.forename: Philippe K
authors.initials: PK
authors.lastname: Zysset
authors.forename: Thomas M
authors.initials: TM
authors.lastname: Stulnig
authors.forename: Peter
authors.initials: P
authors.lastname: Pietschmann
mesh_terms: D015502:Absorptiometry, Photon; D052242:Adiponectin / Q000097:blood; D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D015519:Bone Density / Q000187:drug effects*; D001862:Bone Resorption / Q000000981:diagnostic imaging / Q000378:metabolism*; D001842:Bone and Bones / Q000000981:diagnostic imaging / Q000378:metabolism / Q000648:ultrastructure*; D024042:Collagen Type I / Q000032:analysis; D018752:Diet, Fat-Restricted; D004041:Dietary Fats / Q000008:administration & dosage*; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000097:blood; D008159:Lumbar Vertebrae / Q000000981:diagnostic imaging / Q000378:metabolism / Q000648:ultrastructure; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009765:Obesity / Q000209:etiology*; D015675:Osteocalcin / Q000097:blood
chemical_list: D052242:Adiponectin; D024042:Collagen Type I; D004041:Dietary Fats; D007328:Insulin; D020738:Leptin; D015675:Osteocalcin