甜蜜骨骼:糖尿病中骨改变的发病机制

Sweet Bones: The Pathogenesis of Bone Alteration in Diabetes.

作者信息

Al-Hariri Mohammed

机构信息

Department of Physiology, College of Medicine, University of Dammam, P. O. Box 2114-31451, Dammam, Saudi Arabia.

出版信息

J Diabetes Res. 2016;2016:6969040. doi: 10.1155/2016/6969040. Epub 2016 Sep 29.

Abstract

Diabetic patients have increased fracture risk. The pathogenesis underlying the status of bone alterations in diabetes mellitus is not completely understood but is multifactorial. The major deficits appear to be related to a deficit in mineralized surface area, a decrement in the rate of mineral apposition, deceased osteoid surface, depressed osteoblast activity, and decreased numbers of osteoclasts due to abnormal insulin signaling pathway. Other prominent features of diabetes mellitus are an increased urinary excretion of calcium and magnesium, accumulation of advanced glycation end products, and oxidative stress leading to sweet bones (altered bone's strength, metabolism, and structure). Every diabetic patient should be assessed for risk factors for fractures and osteoporosis. The pathogenesis of the bone alterations in diabetes mellitus as well as their molecular mechanisms needs further study.

摘要

糖尿病患者骨折风险增加。糖尿病患者骨改变状态的潜在发病机制尚未完全明确,但具有多因素性。主要缺陷似乎与矿化表面积不足、矿物质沉积速率降低、类骨质表面减少、成骨细胞活性降低以及由于胰岛素信号通路异常导致破骨细胞数量减少有关。糖尿病的其他显著特征是钙和镁的尿排泄增加、晚期糖基化终产物的积累以及导致骨骼变脆(骨骼强度、代谢和结构改变)的氧化应激。每位糖尿病患者都应评估骨折和骨质疏松症的风险因素。糖尿病患者骨改变的发病机制及其分子机制需要进一步研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/240a/5061963/ee30407c3aa7/JDR2016-6969040.001.jpg

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