Diabetes and Bone

被引:27
作者
Pietschmann, P. [1 ]
Patsch, J. M. [1 ]
Schernthaner, G. [2 ]
机构
[1] Med Univ Vienna, Ctr Pathophysiol Infectiol & Immunol, Dept Pathophysiol & Allergy Res, A-1090 Vienna, Austria
[2] Rudolfstiftung Hosp, Dept Med 1, Vienna, Austria
基金
奥地利科学基金会;
关键词
diabetes mellitus; advanced glycosylation endproducts; osteocalcin; thiazolidinediones; runx2; PPAR gamma; INSULIN-RECEPTOR EXPRESSION; GROWTH FACTOR-I; MINERAL DENSITY; FRACTURE RISK; TRABECULAR BONE; VITAMIN-D; MELLITUS; TYPE-1; ROSIGLITAZONE; OSTEOCALCIN;
D O I
10.1055/s-0030-1262825
中图分类号
R5 [内科学];
学科分类号
100201 [内科学];
摘要
Traditionally, patients with type 1 diabetes were regarded to be at an increased risk of fractures whereas type 2 diabetics were assumed to be protected from fractures since many of them have high bone mineral density. Nevertheless, several clinical studies consistently demonstrated that type 2 diabetes is a paradigm of a disease with an increased risk of fractures in the presence of high bone mass. The pathophysiology of decreased bone strength in diabetes mellitus is multifactorial: insulin deficiency, insulin resistance, osteoblast insufficiency, vitamin D deficiency, formation of advanced glycation end-products in bone, and microvascular complications appear to contribute. Drugs used for the treatment of type 2 diabetes also may influence bone fragility: thiazolidinedione use has been associated with an increased risk of fractures.
引用
收藏
页码:763 / 768
页数:6
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