Diabetes, Collagen, and Bone Quality
Diabetes, Collagen, and Bone Quality
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DOI：
10.1007/s11914-014-0202-7
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发表时间：
2014-06-01
影响因子：
4.3
通讯作者：
Marumo, Keishi
中科院分区：
文献类型：
--
作者：
Saito, Mitsuru;Kida, Yoshikuni;Marumo, Keishi
糖尿病增加骨折的风险，尽管与非糖尿病患者相比，2型糖尿病的特征是正常或高骨矿物质密度（BMD）。1型糖尿病和2型糖尿病的骨折风险增加超出了BMD降低的解释。因此，糖尿病可能会降低骨强度而不会改变BMD。全骨强度由骨密度、结构和质量决定，包括微观结构和组织材料特性。最近的文献表明，糖尿病降低骨材料的性能，而不是BMD。胶原分子间交联在骨强度的表达中起重要作用。胶原交联可分为有益的酶促不成熟的二价和成熟的三价交联以及由糖化和氧化诱导的不利的非酶促交联（晚期糖化终产物：AGEs）。其形成途径和生物学功能有很大不同。不仅高血糖，而且氧化应激诱导酶交联和AGEs形成的减少。本文综述了糖尿病患者骨质量降低的机制，以及血浆或尿液AGEs水平的测定对骨折风险评估的作用。
Diabetes increases risk of fracture, although type 2 diabetes is characterized by normal or high bone mineral density (BMD) compared with the patients without diabetes. The fracture risk of type 1 diabetes as well as type 2 diabetes increases beyond an explained by a decrease of BMD. Thus, diabetes may reduce bone strength without change in BMD. Whole bone strength is determined by bone density, structure, and quality, which encompass the micro-structural and tissue material properties. Recent literature showed that diabetes reduces bone material properties rather than BMD. Collagen intermolecular cross-linking plays an important role in the expression of bone strength. Collagen cross-links can be divided into beneficial enzymatic immature divalent and mature trivalent cross-links and disadvantageous nonenzymatic cross-links (Advanced glycation end products: AGEs) induced by glycation and oxidation. The formation pathway and biological function are quite different. Not only hyperglycemia, but also oxidative stress induces the reduction in enzymatic cross-links and the formation of AGEs. In this review, we describe the mechanism of low bone quality in diabetes and the usefulness of the measurement of plasma or urinary level of AGEs for estimation of fracture risk.