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Circulatory and adipose tissue leptin and adiponectin in relationship to resting energy expenditure in patients with chronic obstructive pulmonary disease

机译:慢性阻塞性肺疾病患者的循环和脂肪组织瘦素和脂联素与静息能量消耗的关系

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Increases in resting energy expenditure (REE) likely contribute to weight loss in various chronic diseases. In chronic obstructive pulmonary disease (COPD), relationships between the ventilatory impairment and increased REE, and between disturbances in adipokines and weight loss were previously described. Therefore, we investigated serum levels and adipose tissue expression of leptin and adiponectin, and their relationships to REE in patients with COPD. In 44 patients with stable COPD (38 male; age 62.3±7.2 years), REE was assessed using indirect calorimetry. Subcutaneous adipose tissue samples were analyzed using realtime PCR. From underweight [n=9; body mass index (BMI) <20.0 kg.m~(-2)], to normal weight-overweight (n=24, BMI=20.0-29.9 kg.m~(-2)) and obese patients (n=11; BMI≥30 kg.m~(-2)), REE adjusted for body weight decreased (32.9±6.1 vs. 26.2±5.8 vs. 23.9±6.6 kcal.kg~(-1).24 h~(-1), p=0.006), serum levels and adipose tissue expression of leptin increased (p<0.001 for both), and serum and adipose tissue adiponectin decreased (p<0.001; p=0.004, respectively). REE was inversely related to serum and adipose tissue leptin (R=-0.547, p<0.001; R=-0.458, p=0.002), and directly to serum adiponectin (R=0.316, p=0.039). Underweight patients had increased REE compared to normal weight-overweight patients, in association with reductions in serum and adipose tissue leptin, and increased serum adiponectin, suggesting a role of adipokines in energy imbalance in COPD-related cachexia.
机译:静息能量消耗(REE)的增加可能会导致各种慢性疾病的体重减轻。在慢性阻塞性肺疾病(COPD)中,通气障碍与REE升高之间,脂肪因子紊乱与体重减轻之间的关系已在以前进行了描述。因此,我们调查了COPD患者血清中瘦素和脂联素的水平和脂肪组织表达,以及它们与REE的关系。在44名COPD稳定的患者中(38名男性;年龄62.3±7.2岁),使用间接量热法评估了REE。使用实时PCR分析皮下脂肪组织样品。体重不足[n = 9;体重指数(BMI)<20.0 kg.m〜(-2)],正常体重超重(n = 24,BMI = 20.0-29.9 kg.m〜(-2))和肥胖患者(n = 11; BMI≥30kg.m〜(-2)),针对体重调整的REE降低了(32.9±6.1 vs. 26.2±5.8 vs.23.9±6.6 kcal.kg〜(-1).24 h〜(-1), p = 0.006),瘦素的血清水平和脂肪组织表达增加(两者均p <0.001),血清和脂肪组织脂联素降低(p <0.001; p = 0.004)。 REE与血清和脂肪组织瘦素呈负相关(R = -0.547,p <0.001; R = -0.458,p = 0.002),而与血清脂联素呈负相关(R = 0.316,p = 0.039)。与正常体重超重患者相比,体重过轻患者的REE增加,同时血清和脂肪组织瘦素减少,血清脂联素增加,提示脂肪因子在COPD相关恶病质的能量失衡中发挥作用。

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