Increased bone resorption and impaired bone microarchitecture in short-term and extended high-fat diet-induced obesity.
Increased bone resorption and impaired bone microarchitecture in short-term and extended high-fat diet-induced obesity.
复制标题
DOI：
10.1016/j.metabol.2009.11.023
复制
发表时间：
2011-03
期刊：
影响因子：
--
通讯作者：
Pietschmann P
中科院分区：
文献类型：
--
作者：
Patsch JM;Kiefer FW;Varga P;Pail P;Rauner M;Stupphann D;Resch H;Moser D;Zysset PK;Stulnig TM;Pietschmann P
虽然肥胖传统上被认为是骨质疏松症的低风险条件，这一经典观点最近受到质疑。本研究的目的是评估高脂饮食诱导的肥胖小鼠模型的骨微结构和转换。将7周龄雄性C57 BL/6 J小鼠（n = 18）随机分为3个饮食组。三分之一（n = 6）接受低脂饮食24周，三分之一保持延长的高脂饮食（eHF），其余的在处死前3周从低脂食物转换为高脂食物（sHF）。测定血清胰岛素、瘦素、脂联素、骨钙素和I型胶原交联端肽（CTX）水平。此外，骨微结构进行了分析，微计算机断层扫描和腰椎骨密度进行了评估，双能X线吸收。肥胖动物的CTX、体重、胰岛素和瘦素显著升高（sHF：+48%、+24%、+265%和+102%; eHF：+43%、+52%、+761%和+292%）。CTX、体重、胰岛素、瘦素与骨密度、骨体积呈负相关。有趣的是，短期高脂肪食物引起的骨质流失与长期高脂肪食物相似。sHF和eHF的骨量分别减少了12%和19%。与低脂饮食的对照小鼠相比，骨密度分别降低了25%（sHF）和27%（eHF）。通过结构模型指数评估，骨微结构在高脂肪挑战后从板状外观变为杆状外观。骨小梁和皮质厚度未受影响。短期和长期高脂饮食诱导的肥胖导致雄性C57 BL/6 J小鼠显著的骨丢失，主要是因为骨小梁结构的再吸收变化。
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.
登录
查看更多内容
影响因子：
4.1
作者：
Beamer, WG;Donahue, LR;Baylink, DJ
通讯作者：
Baylink, DJ
影响因子：
4
作者：
Ahmed, LA;Schirmer, H;Joakimsen, RMJ
通讯作者：
Joakimsen, RMJ
影响因子：
6.2
作者：
Burge, Russel;Dawson-Hughes, Bess;Tosteson, Anna
通讯作者：
Tosteson, Anna
影响因子：
4
作者：
Looker, A. C.;Flegal, K. M.;Melton, L. J., III
通讯作者：
Melton, L. J., III
影响因子：
64.5
作者：
Lee, Na Kyung;Sowa, Hideaki;Karsenty, Gerard
通讯作者：
Karsenty, Gerard