Leni and Peter W. May Department of Orthopaedics, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Department of Biomedical Engineering, Center for Biotechnology and Interdisciplinary Studies, Rensselaer Polytechnic Institute, Troy, NY, USA.
J Bone Miner Res. 2018 Mar;33(3):437-448. doi: 10.1002/jbmr.3321. Epub 2017 Nov 27.
Back pain is a leading cause of global disability that can arise from vertebral fracture and osteoporosis. Although poor general health and obesity are among the strongest risk factors for back pain, there is remarkably little known about how diet influences spinal diseases. Advanced glycation end-products (AGEs) are implicated in increased fracture risk, yet no studies investigated how dietary AGEs affect spinal health. We tested the hypothesis that high dietary AGE ingestion will diminish vertebral structure and function in a sex- and age-dependent manner. Female and male mice were fed low-AGE (L-AGE) or high-AGE (H-AGE) isocaloric diets for 6 and 18 months and multiple measurements of bone structure and function were taken. AGE levels in serum and cortical vertebrae were increased only for 6-month-old H-AGE female mice while blood glucose and body weight remained normal for all animals. When fed an H-AGE diet, 6-month-old female mice had inferior vertebral trabecular structure with decreased bone mineral density (BMD) and bone volume fraction. Biomechanical testing and analytical modeling further showed functional deterioration in 6-month-old H-AGE females with reduced shear and compression moduli, and maximum load to failure. At 18 months, H-AGE mice of both sexes had significant but small decreases in cortical BMD and thickness, yet functional biomechanical behaviors were not distinguishable from other aging changes. We conclude that an H-AGE diet, without diabetic or overweight conditions, diminished vertebral microstructure, mechanical behaviors, and fracture resistance in young female mice in a manner suggesting accelerated bone aging. © 2017 American Society for Bone and Mineral Research.
背痛是导致全球残疾的主要原因之一，它可能由椎体骨折和骨质疏松症引起。尽管一般健康状况不佳和肥胖是背痛的最强危险因素之一，但人们对饮食如何影响脊柱疾病知之甚少。晚期糖基化终产物（AGEs）与骨折风险增加有关，但尚无研究调查饮食 AGEs 如何影响脊柱健康。我们假设高饮食 AGE 摄入将以性别和年龄依赖的方式减少椎体结构和功能。雌性和雄性小鼠分别用低 AGE（L-AGE）或高 AGE（H-AGE）等热量饮食喂养 6 个月和 18 个月，并对骨结构和功能进行了多项测量。仅在 6 个月大的 H-AGE 雌性小鼠中，血清和皮质椎体中的 AGE 水平升高，而所有动物的血糖和体重均保持正常。当喂食 H-AGE 饮食时，6 个月大的雌性小鼠的椎体小梁结构较差，骨矿物质密度（BMD）和骨体积分数降低。生物力学测试和分析模型进一步表明，6 个月大的 H-AGE 雌性小鼠的功能恶化，剪切和压缩模量以及最大失效负荷降低。在 18 个月时，雌雄 H-AGE 小鼠的皮质 BMD 和厚度均有显著但较小的下降，但功能生物力学行为与其他衰老变化无法区分。我们得出结论，在没有糖尿病或超重的情况下，H-AGE 饮食会使年轻雌性小鼠的椎体微结构、机械性能和抗骨折能力降低，这表明骨老化加速。© 2017 美国骨骼与矿物质研究协会。
