胰岛素抵抗致骨强度下降的机制研究  

Research progress in the mechanism of insulin resistance-induced decrease in bone strength

作　　者：程秀宇 高飞[2] CHENG Xiuyu;GAO Fei(Shanxi Medical University,Taiyuan 030000;The First Hospital of Shanxi Medical University,Taiyuan 030000,China)

机构地区：[1]山西医科大学,山西太原030000 [2]山西医科大学第一医院,山西太原030000

出　　处：《中国骨质疏松杂志》2023年第6期926-931,共6页Chinese Journal of Osteoporosis

摘　　要：胰岛素抵抗是2型糖尿病重要的发病机制之一,随着胰岛素抵抗程度的增加,骨成长和骨重塑过程变化导致骨折风险增加。在胰岛素抵抗的患者中,并不完全表现为骨密度减少的骨质疏松症,也可能表现为正常或者高骨密度,导致2型糖尿病患者骨密度未见明显异常而骨折风险增加,这可能是由于成骨细胞和破骨细胞对胰岛素敏感度降低或者胰岛素抵抗导致的低度炎症、维生素D降低、骨细胞间隙矿化等因素影响骨形成和骨吸收的平衡。胰岛素抵抗导致骨强度下降的机制有待充分阐明以期其指导胰岛素抵抗患者的抗骨质疏松治疗。Insulin resistance is one of the important pathogenic mechanisms of type 2 diabetes.As the degree of insulin resistance increases,changes in bone growth and bone remodeling process lead to an increased risk of fractures.In patients with insulin resistance,osteoporosis that does not completely manifest as decreased bone density,may also manifest as normal or high bone density,resulting in no obvious abnormalities in bone mineral density and an increased risk of fracture in patients with type 2 diabetes.This may be due to reduced osteoblast and osteoclast sensitivity to insulin or low inflammation caused by insulin resistance,decreased vitamin D,mineralization of osteocyte spaces,and other factors affecting bone formation and bone resorption.The mechanism by which insulin resistance leads to bone strength loss needs to be fully elucidated in order to guide anti-osteoporosis therapy in patients with insulin resistance.

关 键 词：胰岛素抵抗 2型糖尿病 骨质疏松 骨强度 

分 类 号：R681[医药卫生—骨科学] R587[医药卫生—外科学]