scholarly journals Circulatory and Adipose Tissue Leptin and Adiponectin in Relationship to Resting Energy Expenditure in Patients With Chronic Obstructive Pulmonary Disease

2012 ◽  
pp. 469-480 ◽  
Author(s):  
M. BRÚSIK ◽  
J. UKROPEC ◽  
P. JOPPA ◽  
B. UKROPCOVÁ ◽  
P. SKYBA ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Weight Loss ◽  
Adipose Tissue ◽  
Energy Expenditure ◽  
Resting Energy Expenditure ◽  
Serum Levels ◽  
Tissue Expression ◽  
Normal Weight ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease

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 real-time 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.

scholarly journals Metabolic Phenotype and Adipose Tissue Inflammation in Patients with Chronic Obstructive Pulmonary Disease

2010 ◽  
Vol 2010 ◽  
pp. 1-9 ◽  
Author(s):  
Peter Skyba ◽  
Jozef Ukropec ◽  
Pavol Pobeha ◽  
Barbara Ukropcova ◽  
Pavol Joppa ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Pulmonary Disease ◽  
Normal Weight ◽  
Cell Surface Receptor ◽  
Metabolic Phenotype ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Tnf Α

Potential links between metabolic derangements and adipose tissue (AT) inflammation in patients with chronic obstructive pulmonary disease (COPD) are unexplored. We investigated AT expressions of interleukin (IL)-6, tumor necrosis factor (TNF)-α, CD68 (macrophage cell surface receptor), caspase-3, and Bax, and their relationships to the metabolic phenotype in nine cachectic, 12 normal-weight, 12 overweight, and 11 obese patients with COPD (age62.3±7.2years). With increasing body mass index, increases in AT expressions of IL-6, TNF-α, and CD68 were observed (P<.001;P=.005;P<.001, resp.), in association with reduced insulin sensitivity (P<.001). No differences were observed between cachectic and normal-weight patients in AT expressions of inflammatory or proapoptotic markers. Adipose tissue CD68 and TNF-α expressions predicted insulin sensitivity independently of known confounders (P=.005;P=.025;R2=0.840). Our results suggest that AT inflammation in obese COPD patients relates to insulin resistance. Cachectic patients remain insulin sensitive, with no AT upregulation of inflammatory or proapoptotic markers.

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