Metabolic Phenotype and Adipose Tissue Inflammation in Patients with Chronic Obstructive Pulmonary Disease. (21st December 2010)

• Record Type: Journal Article
• Authors: Skyba, Peter; Ukropec, Jozef; Pobeha, Pavol; Ukropcova, Barbara; Joppa, Pavol; Kurdiova, Timea; Stroffekova, Katarina; Brusik, Miroslav; Klimes, Iwar; Tkac, Ivan; Gasperikova, Daniela; Tkacova, Ruzena
• Other Names: Touyz Rhian Academic Editor.
• Is Part Of: Mediators of inflammation. Volume 2010(2010)
• Publication Date: 2010-12-21
• Subjects: Inflammation -- Mediators -- Periodicals; Biological response modifiers -- Periodicals; Inflammation (Pathologie) -- Médiateurs; Immunomodulateurs; Biological response modifiers; Inflammation -- Mediators; Immunology; Autacoids; Immunologic Factors; Cell Adhesion Molecules; Cell Communication; Cytokines; Inflammation; Periodicals; Electronic journals; 616.0473
• DOI: 10.1155/2010/173498
• Languages: English
• ISSNs: 0962-9351

Abstract

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.