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ファイル
言語
英語
属性
総説
著者
山本 昌弘 島根大学医学部内科学第一
杉本 利嗣 島根大学医学部内科学第一
内容記述(抄録等)
Diabetic patients have a higher fracture risk than expected by their bone mineral density (BMD). Poor bone quality is the most suitable and explainable cause for the elevated fracture risk in this population. Advanced glycation end products (AGEs), which are diverse compounds generated via a non-enzymatic reaction between reducing sugars and amine residues, physically affect the properties of the bone material, one of a component of bone quality, through their accumulation in the bone collagen fibers. On the other hand, these compounds biologically act as agonists for these receptors for AGEs (RAGE) and suppress bone metabolism. The concentrations of AGEs and endogenous secretory RAGE, which acts as a “decoy receptor” that inhibits the AGEs-RAGE signaling axis, are associated with fracture risk in a BMD-independent manner. AGEs are closely associated with the pathogenesis of this unique clinical manifestation through physical and biological mechanisms in patients with diabetes mellitus.
主題
Fracture
Bone quality
Material properties
Pentosidine
Crosslink
Receptor for advanced glycation end products (RAGE)
掲載誌名
Current osteoporosis reports
14
6
開始ページ
320
終了ページ
326
ISSN
15441873
発行日
2016-12
DOI
PubMed ID
出版者
Current Science
資料タイプ
学術雑誌論文
ファイル形式
PDF
権利関係
© The Author(s) 2016. This article is published with open access at Springerlink.com
著者版/出版社版
出版社版
部局
医学部