Walsh Jennifer S, Vilaca Tatiane
Academic Unit of Bone Metabolism, Mellanby Centre for Bone Research, University of Sheffield, Sheffield, UK.
Calcif Tissue Int. 2017 May;100(5):528-535. doi: 10.1007/s00223-016-0229-0. Epub 2017 Mar 9.
In an increasingly obese and ageing population, type 2 diabetes (T2DM) and osteoporotic fracture are major public health concerns. Understanding how obesity and type 2 diabetes modulate fracture risk is important to identify and treat people at risk of fracture. Additionally, the study of the mechanisms of action of obesity and T2DM on bone has already offered insights that may be applicable to osteoporosis in the general population. Most available evidence indicates lower risk of proximal femur and vertebral fracture in obese adults. However the risk of some fractures (proximal humerus, femur and ankle) is higher, and a significant number fractures occur in obese people. BMI is positively associated with BMD and the mechanisms of this association in vivo may include increased loading, adipokines such as leptin, and higher aromatase activity. However, some fat depots could have negative effects on bone; cytokines from visceral fat are pro-resorptive and high intramuscular fat content is associated with poorer muscle function, attenuating loading effects and increasing falls risk. T2DM is also associated with higher bone mineral density (BMD), but increased overall and hip fracture risk. There are some similarities between bone in obesity and T2DM, but T2DM seems to have additional harmful effects and emerging evidence suggests that glycation of collagen may be an important factor. Higher BMD but higher fracture risk presents challenges in fracture prediction in obesity and T2DM. Dual energy X-ray absorptiometry underestimates risk, standard clinical risk factors may not capture all relevant information, and risk is under-recognised by clinicians. However, the limited available evidence suggests that osteoporosis treatment does reduce fracture risk in obesity and T2DM with generally similar efficacy to other patients.
在日益肥胖和老龄化的人群中,2型糖尿病(T2DM)和骨质疏松性骨折是主要的公共卫生问题。了解肥胖和2型糖尿病如何调节骨折风险对于识别和治疗有骨折风险的人群至关重要。此外,对肥胖和T2DM对骨骼作用机制的研究已经提供了一些可能适用于普通人群骨质疏松症的见解。大多数现有证据表明肥胖成年人股骨近端和椎体骨折的风险较低。然而,某些骨折(肱骨近端、股骨和踝关节)的风险较高,并且肥胖人群中发生大量骨折。BMI与骨密度呈正相关,这种体内关联的机制可能包括负荷增加、瘦素等脂肪因子以及较高的芳香化酶活性。然而,一些脂肪储存部位可能对骨骼有负面影响;内脏脂肪产生的细胞因子具有促进骨吸收的作用,而肌肉内脂肪含量高与较差的肌肉功能相关,会减弱负荷效应并增加跌倒风险。T2DM也与较高的骨矿物质密度(BMD)相关,但总体骨折风险和髋部骨折风险增加。肥胖和T2DM患者的骨骼存在一些相似之处,但T2DM似乎有额外的有害影响,新出现的证据表明胶原蛋白糖基化可能是一个重要因素。较高的骨密度但较高的骨折风险给肥胖和T2DM患者的骨折预测带来了挑战。双能X线吸收法会低估风险,标准临床风险因素可能无法涵盖所有相关信息,临床医生对风险的认识不足。然而,有限的现有证据表明,骨质疏松症治疗确实可以降低肥胖和T2DM患者的骨折风险,其疗效与其他患者总体相似。