Department of Respiratory Medicine, and Tuberculosis, P.J. Safarik University, Kosice, Slovakia.
Bone. 2011 May 1;48(5):1008-14. doi: 10.1016/j.bone.2011.02.017. Epub 2011 Mar 1.
The role of fat-bone interactions in the pathogenesis of osteoporosis in chronic obstructive pulmonary disease (COPD) is poorly understood. Our aim was to investigate expressions of leptin and osteoprotegerin (OPG) in the adipose tissue, and their relationships to osteoporosis in patients with COPD.
In 39 patients with stable COPD, bone mineral density (BMD) and body composition was assessed by Dual Energy X-Ray Absorptiometry. Serum leptin was determined by the enzyme-linked immunosorbent assay, and bone turnover markers osteocalcin and β-crosslaps by the electrochemiluminiscence immunoassays. Subcutaneous adipose tissue samples were analyzed using real-time PCR.
Twenty-one patients without, and 18 with osteoporosis were enrolled (35 men; age 62.2 ± 7.3years). Compared to patients without osteoporosis, those with the disease had significantly lower serum levels and adipose tissue expressions of leptin, in association with increased serum β-crosslaps (p=0.028, p=0.034, p=0.022, respectively). Log adipose tissue leptin was inversely related to serum β-crosslaps (p=0.015), and directly to serum leptin (p<0.001) and to the total, femoral, and lumbar BMD and T-score (p<0.02 for all relationships). Adipose tissue OPG expression was related to all variables of bone density except for lumbar BMD and T-score (p<0.05 for all relationships). Log adipose tissue leptin and OPG expressions predicted femoral T-score independently of age, gender and pulmonary function (p<0.001, adjusted R(2)=0.383; p=0.008, adjusted R(2)=0.301, respectively). Introducing body mass (or fat mass) index into these models eliminated independent predictive value of leptin and OPG expressions.
Our results suggest that adipose tissue leptin and OPG expressions are related to osteoporosis in patients with COPD, and appear to act as mediators between fat mass and BMD.
脂肪-骨骼相互作用在慢性阻塞性肺疾病（COPD）骨质疏松症的发病机制中的作用尚不清楚。我们的目的是研究瘦素和骨保护素（OPG）在脂肪组织中的表达及其与 COPD 患者骨质疏松症的关系。
在 39 例稳定期 COPD 患者中，通过双能 X 射线吸收法评估骨矿物质密度（BMD）和身体成分。通过酶联免疫吸附试验测定血清瘦素，通过电化学发光免疫测定法测定骨转换标志物骨钙素和β-交联胶原。使用实时 PCR 分析皮下脂肪组织样本。
共纳入 21 例无骨质疏松症和 18 例骨质疏松症患者（35 名男性；年龄 62.2±7.3 岁）。与无骨质疏松症患者相比，患有该疾病的患者血清瘦素水平和脂肪组织表达水平明显降低，同时血清β-交联胶原水平升高（p=0.028，p=0.034，p=0.022）。脂肪组织瘦素的对数与血清β-交联胶原呈负相关（p=0.015），与血清瘦素直接相关（p<0.001），与总、股骨和腰椎 BMD 和 T 评分直接相关（所有关系 p<0.02）。脂肪组织 OPG 表达与骨密度的所有变量均相关，除了腰椎 BMD 和 T 评分（所有关系 p<0.05）。脂肪组织瘦素和 OPG 表达的对数可独立于年龄、性别和肺功能预测股骨 T 评分（p<0.001，调整 R(2)=0.383；p=0.008，调整 R(2)=0.301）。将体重（或脂肪量）指数引入这些模型中，消除了瘦素和 OPG 表达的独立预测值。
我们的结果表明，脂肪组织瘦素和 OPG 的表达与 COPD 患者的骨质疏松症有关，并且似乎作为脂肪量和 BMD 之间的介质起作用。
