Increased bone resorption and impaired bone microarchitecture in short-term and extended high-fat diet-induced obesity |
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Authors: | Janina M. Patsch Florian W. Kiefer Pamela Pail Daniela Stupphann Doris Moser Thomas M. Stulnig |
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Affiliation: | a Division of Cellular and Molecular Pathophysiology, Department of Pathophysiology, Center of Physiology, Pathophysiology and Immunology, Medical University Vienna, A-1090 Vienna, Austriab Division of Neuroradiology and Musculoskeletal Radiology, Department of Radiology, Medical University Vienna, A-1090 Vienna, Austriac Clinical Division of Endocrinology and Metabolism, Department of Internal Medicine III, Medical University Vienna, A-1090 Vienna, Austriad Institute of Lightweight Design and Structural Biomechanics, Vienna University of Technology, A-1040 Vienna, Austriae Division of Endocrinology, Diabetes, and Bone Diseases, Department of Medicine III, Technical University Dresden, Dresden, Germanyf Medical Department II, St. Vincent Hospital Vienna, A-1060 Vienna, Austriag Department of Cranio-, Maxillofacial and Oral Surgery, Medical University Vienna, A-1090 Vienna, Austria |
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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. |
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