Chun-Rong Ju1, Rong-Chang Chen. 1. State Key Lab of Respiratory Disease, First Affiliated Hospital of Guangzhou Medical College, Guangdong 510012, China.
Abstract
INTRODUCTION: It is well confirmed that myostatin is a negative regulator of skeletal muscle mass and implicated in several diseases involved in muscle wasting and cachexia. Skeletal muscle wasting is an important systemic manifestation of chronic obstructive pulmonary disease (COPD), while the expression of circulating myostatin in COPD remains unclear. The aim of this study was to investigate the expression of circulating myostatin and its relationship with skeletal muscle wasting in COPD. METHODS: Seventy-one patients with stable COPD and sixty age-matched, healthy control subjects participated in the study. Total skeletal muscle mass (SMM) were calculated according to a validated formula by using age and anthropometric measurements. Serum levels of myostatin, tumor necrosis factor (TNF)-α and interleukin-6 were determined by ELISA. RESULTS: Serum myostatin levels were significantly elevated in COPD patients when compared to controls [(11.85 ± 4.01) ng/ml vs. (7.46 ± 2.21) ng/ml, p < 0.01], while total SMM was significantly decreased in COPD patients when compared to controls [(20.81 ± 1.74) kg vs. (27.31 ± 2.18) kg for male, and (11.70 ± 0.56) kg vs. (19.89 ± 1.47) kg for female] (both p < 0.05). Regression correlation analysis on all COPD patients showed that serum myostatin levels weren't significantly correlated with SMM, but correlated with TNF-α levels (R(2) = 0.042, p = 0.048). However, when stratified for gender, serum myostatin levels were correlated inversely both with SMM (R(2) = 0.20, p = 0.000) and with BMI (R(2) = 0.084, p = 0.019) in subgroup of male patients. CONCLUSION: This study demonstrates that circulating myostatin levels are elevated in COPD and related to SMM in male patients, suggesting that myostatin contributes to skeletal muscle wasting in COPD.
INTRODUCTION: It is well confirmed that myostatin is a negative regulator of skeletal muscle mass and implicated in several diseases involved in muscle wasting and cachexia. Skeletal muscle wasting is an important systemic manifestation of chronic obstructive pulmonary disease (COPD), while the expression of circulating myostatin in COPD remains unclear. The aim of this study was to investigate the expression of circulating myostatin and its relationship with skeletal muscle wasting in COPD. METHODS: Seventy-one patients with stable COPD and sixty age-matched, healthy control subjects participated in the study. Total skeletal muscle mass (SMM) were calculated according to a validated formula by using age and anthropometric measurements. Serum levels of myostatin, tumor necrosis factor (TNF)-α and interleukin-6 were determined by ELISA. RESULTS: Serum myostatin levels were significantly elevated in COPD patients when compared to controls [(11.85 ± 4.01) ng/ml vs. (7.46 ± 2.21) ng/ml, p < 0.01], while total SMM was significantly decreased in COPD patients when compared to controls [(20.81 ± 1.74) kg vs. (27.31 ± 2.18) kg for male, and (11.70 ± 0.56) kg vs. (19.89 ± 1.47) kg for female] (both p < 0.05). Regression correlation analysis on all COPD patients showed that serum myostatin levels weren't significantly correlated with SMM, but correlated with TNF-α levels (R(2) = 0.042, p = 0.048). However, when stratified for gender, serum myostatin levels were correlated inversely both with SMM (R(2) = 0.20, p = 0.000) and with BMI (R(2) = 0.084, p = 0.019) in subgroup of male patients. CONCLUSION: This study demonstrates that circulating myostatin levels are elevated in COPD and related to SMM in male patients, suggesting that myostatin contributes to skeletal muscle wasting in COPD.
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