Plasma and muscle amino acid levels in relation to resting energy expenditure and inflammation in stable chronic obstructive pulmonary disease.
In patients with chronic obstructive pulmonary disease (COPD), muscle wasting can occur independently of fat loss, suggesting disturbances in protein metabolism. In order to provide more insight in amino-acid (AA) metabolism in patients with stable COPD, we examined arterial plasma and anterior tibialis muscle AA levels, comparing 12 COPD patients with eight age-matched healthy control subjects. We also studied relationships between AA levels, the acute phase response as measured by lipopolysaccharide-binding protein (LBP), and resting energy expenditure (REE). In contrast to findings in acute diseases associated with muscle wasting, we found increased muscle glutamine (GLN) levels in our patient group (mean +/- SEM = 10,782 +/- 770 versus 7,844 +/- 293 micromol/kg wet weight, p < 0. 01). Furthermore, muscle arginine, ornithine, and citrulline were significantly increased in the patient group, whereas glutamic acid was decreased. In plasma, the sum of all AA (SumAA) was decreased in the patient group (2,595 +/- 65 versus 2,894 +/- 66 micromol/L, p < 0.01), largely because of decreased levels of alanine (254 +/- 10 versus 375 +/- 25 micromol/L, p < 0.0001), GLN (580 +/- 17 versus 641 +/- 17 micromol/L, p < 0.05), and glutamic acid (91 +/- 5 versus 130 +/- 10 micromol/L, p < 0.01). LBP levels were increased in COPD patients as compared with controls (11.7 +/- 4.5 versus 8.6 +/- 1.0 mg/L, p < 0.05), and showed a positive correlation with REE (r = 0. 49, p = 0.03), a negative correlation with the SumAA in plasma (r = -0.76, p < 0.0001), and no correlation with muscle AA levels. In conclusion, various disturbances in plasma and muscle AA levels were found in COPD patients. A relationship between the observed decreased plasma AA levels and inflammation was suggested.
Pouw
E M
EM
Departments of Pulmonology and Surgery, Maastricht University, Maastricht, and Asthmacentre Hornerheide, Horn, The Netherlands.
Schols
A M
AM
Deutz
N E
NE
Wouters
E F
EF
D000209:Acute-Phase Proteins / Q000032:analysis; D000210:Acute-Phase Reaction / Q000378:metabolism / Q000473:pathology; D000273:Adipose Tissue / Q000473:pathology; D000368:Aged; D000409:Alanine / Q000032:analysis / Q000097:blood; D000596:Amino Acids / Q000032:analysis / Q000097:blood*; D001120:Arginine / Q000032:analysis / Q000097:blood; D002352:Carrier Proteins / Q000032:analysis; D016022:Case-Control Studies; D002956:Citrulline / Q000032:analysis / Q000097:blood; D004734:Energy Metabolism; D018698:Glutamic Acid / Q000032:analysis / Q000097:blood; D005973:Glutamine / Q000032:analysis / Q000097:blood; D006801:Humans; D008070:Lipopolysaccharides / Q000032:analysis; D008173:Lung Diseases, Obstructive / Q000378:metabolism*; D008562:Membrane Glycoproteins; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000737:chemistry* / Q000378:metabolism / Q000473:pathology; D009135:Muscular Diseases / Q000378:metabolism / Q000473:pathology; D009952:Ornithine / Q000032:analysis / Q000097:blood; D011506:Proteins / Q000378:metabolism; D012146:Rest / Q000502:physiology; D000099231:Lipopolysaccharide-Binding Protein
D000209:Acute-Phase Proteins; D000409:Alanine; D000596:Amino Acids; D001120:Arginine; D002352:Carrier Proteins; D002956:Citrulline; D018698:Glutamic Acid; D005973:Glutamine; D008070:Lipopolysaccharides; D008562:Membrane Glycoproteins; D009952:Ornithine; D011506:Proteins; D000099231:Lipopolysaccharide-Binding Protein