• Medientyp: E-Artikel
  • Titel: Negative Influence of a Long-Term High-Fat Diet on Murine Bone Architecture
  • Beteiligte: Fehrendt, Hinrich; Linn, Thomas; Hartmann, Sonja; Szalay, Gabor; Heiss, Christian; Schnettler, Reinhard; Lips, Katrin Susanne
  • Erschienen: Hindawi Limited, 2014
  • Erschienen in: International Journal of Endocrinology, 2014 (2014), Seite 1-9
  • Sprache: Englisch
  • DOI: 10.1155/2014/318924
  • ISSN: 1687-8337; 1687-8345
  • Schlagwörter: Endocrine and Autonomic Systems ; Endocrinology ; Endocrinology, Diabetes and Metabolism
  • Entstehung:
  • Anmerkungen:
  • Beschreibung: <jats:p>A correlation between obesity and bone metabolism is strongly assumed because adipocytes and osteoblasts originate from the same precursor cells and their differentiation is conversely regulated by the same factors. It is controversially discussed if obesity protects bone or leads to loss of bone mass. Thus, the aim of the present study was to investigate the influence of diet-induced mild obesity (11% increased body weight compared to control) on bone microstructure in mice. Four-week-old male C57BL/6J mice received a high-fat diet (HFD, 60% kcal from fat) and were analyzed by means of dual X-ray absorptiometry, histological methods, real-time RT-PCR, and transmission electron microscopy in comparison to control animals (10% kcal from fat). The cancellous bone mass, collagen 1<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M1"><mml:mrow><mml:mi>α</mml:mi></mml:mrow></mml:math>1 expression, amount of osteoid, and cohesion of cells via cell-to-cell contacts decreased in HFD mice whereas the bone mineral density and the amount of osteoblasts and osteoclasts were not modified. The amount of apoptotic osteocytes was increased in HFD mice in comparison to controls. We conclude that moderately increased body weight does not protect bone architecture from age-dependent degeneration. By contrast, bone microstructure is negatively affected and reduced maintenance of cell-cell contacts may be one of the underlying mechanisms.</jats:p>
  • Zugangsstatus: Freier Zugang