Abstract
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 (age 62.3 ± 7.2 years). 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; R(2) = 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.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Adipose Tissue / pathology*
-
Aged
-
Antigens, CD / genetics
-
Antigens, Differentiation, Myelomonocytic / genetics
-
Cachexia / complications
-
Cachexia / genetics
-
Cachexia / metabolism
-
Cachexia / pathology
-
Caspase 3 / genetics
-
Female
-
Gene Expression
-
Humans
-
Inflammation / pathology*
-
Inflammation Mediators / metabolism*
-
Insulin Resistance / physiology
-
Interleukin-6 / genetics
-
Male
-
Metabolic Syndrome / complications
-
Metabolic Syndrome / genetics
-
Metabolic Syndrome / metabolism
-
Middle Aged
-
Obesity / complications
-
Obesity / genetics
-
Obesity / metabolism
-
Obesity / pathology
-
Overweight / complications
-
Overweight / genetics
-
Overweight / metabolism
-
Overweight / pathology
-
Panniculitis / complications
-
Panniculitis / genetics
-
Panniculitis / metabolism
-
Panniculitis / pathology
-
Phenotype
-
Pulmonary Disease, Chronic Obstructive / complications
-
Pulmonary Disease, Chronic Obstructive / genetics
-
Pulmonary Disease, Chronic Obstructive / metabolism*
-
Pulmonary Disease, Chronic Obstructive / pathology*
-
Receptors, Tumor Necrosis Factor, Type I / genetics
-
Tumor Necrosis Factor-alpha / genetics
-
bcl-2-Associated X Protein / genetics
Substances
-
Antigens, CD
-
Antigens, Differentiation, Myelomonocytic
-
BAX protein, human
-
CD68 antigen, human
-
IL6 protein, human
-
Inflammation Mediators
-
Interleukin-6
-
Receptors, Tumor Necrosis Factor, Type I
-
TNFRSF1A protein, human
-
Tumor Necrosis Factor-alpha
-
bcl-2-Associated X Protein
-
CASP3 protein, human
-
Caspase 3