Karakas S, Karadag F, Karul A B, Gurgey O, Gurel S, Guney E, Cildag O
Department of Anatomy, School of Medicine, Adnan Menderes University, Aydin, Turkey.
Int J Clin Pract. 2005 Oct;59(10):1167-70. doi: 10.1111/j.1368-5031.2005.00567.x.
Nutritional depletion and weight loss are two features of chronic obstructive pulmonary disease (COPD), and the association between low body mass index (BMI) and poor prognosis in patients with COPD is a common clinical observation. Mechanisms of weight loss are still unclear in COPD. Excessive energy expenditure partly due to increased work of breathing was shown, but other mechanisms have been searched for. Leptin is a hormone secreted by adipocytes that plays an important role in energy homeostasis and regulates body weight through control of appetite and energy expenditure. The aim of this study was to evaluate the association of circulating leptin levels and measures of body composition in COPD patients. Thirty male COPD outpatients (mean age 66.3 +/- 8.4) and 20 controls (mean age 65.9 +/- 10.8) were included in the study. After standard spirometry and body composition measurements, serum leptin concentration was measured by ELISA assay. COPD patients were grouped according to BMI. Mean BMI was 19.01 +/- 2.26 kg/m2 in group 1 (COPD patients with low BMI), 26.85 +/- 4.51 in group 2 COPD (COPD patients with normal/high BMI) and 27.64 +/- 2.75 kg/m2 in healthy controls (group 3). Mean serum leptin concentration was 1.41 +/- 1.86 ng/ml in group 1, 2.60 +/- 1.38 ng/ml in group 2 and 2.82 +/- 1.46 ng/ml in group 3 (p = 0.002). Leptin correlated to not only BMI but also body weight, waist circumference, triceps and biceps skinfold thickness and body fat percent (p < 0.05 for all). Results of this study suggest that the cause of weight loss is not increased circulating leptin in COPD. Instead, leptin remains regulated in COPD and further decreased in patients with low BMI, probably as a compensatory mechanism to preserve body fat content, which should be evaluated in further studies.
营养耗竭和体重减轻是慢性阻塞性肺疾病（COPD）的两个特征，而低体重指数（BMI）与COPD患者预后不良之间的关联是常见的临床观察结果。COPD患者体重减轻的机制仍不清楚。已表明部分由于呼吸功增加导致能量消耗过多，但也一直在寻找其他机制。瘦素是一种由脂肪细胞分泌的激素，在能量稳态中起重要作用，并通过控制食欲和能量消耗来调节体重。本研究的目的是评估COPD患者循环瘦素水平与身体成分测量值之间的关联。该研究纳入了30名男性COPD门诊患者（平均年龄66.3±8.4岁）和20名对照者（平均年龄65.9±10.8岁）。在进行标准肺功能测定和身体成分测量后，采用酶联免疫吸附测定法测量血清瘦素浓度。COPD患者根据BMI进行分组。第1组（低BMI的COPD患者）的平均BMI为19.01±2.26kg/m²，第2组COPD（正常/高BMI的COPD患者）为26.85±4.51，健康对照组（第3组）为27.64±2.75kg/m²。第1组的平均血清瘦素浓度为1.41±1.86ng/ml，第2组为2.60±1.38ng/ml，第3组为2.82±1.46ng/ml（p = 0.002）。瘦素不仅与BMI相关，还与体重、腰围、肱三头肌和肱二头肌皮褶厚度以及体脂百分比相关（所有p均<0.05）。本研究结果表明，COPD患者体重减轻的原因不是循环瘦素增加。相反，COPD患者的瘦素仍受调节，且在低BMI患者中进一步降低，这可能是一种保存身体脂肪含量的代偿机制，应在进一步研究中进行评估。
