Metabolic profiles among COPD and controls in the CanCOLD population-based cohort

Abstract

A high prevalence of intermediate cardiometabolic risk factors and obesity in chronic obstructive pulmonary disease (COPD) has suggested the existence of pathophysiological links between hypertriglyceridemia, insulin resistance, visceral adiposity, and hypoxia or impaired pulmonary function. However, whether COPD contributes independently to the development of these cardiometabolic risk factors remains unclear. Our objective was to compare ectopic fat and metabolic profiles among representative individuals with COPD and control subjects and to evaluate whether the presence of COPD alters the metabolic risk profile. Study participants were randomly selected from the general population and prospectively classified as non-COPD controls and COPD, according to the Global Initiative for Chronic Obstructive Lung Disease classification. The metabolic phenotype, which consisted of visceral adipose tissue area, metabolic markers including homeostasis model assessment of insulin resistance (HOMA-IR), and blood lipid profile, was obtained in 144 subjects with COPD and 119 non-COPD controls. The metabolic phenotype was similar in COPD and controls. The odds ratios for having pathologic values for HOMA-IR, lipids and visceral adipose tissue area were similar in individuals with COPD and control subjects in multivariate analyses that took into account age, sex, body mass index, tobacco status and current medications. In a population-based cohort, no difference was found in the metabolic phenotype, including visceral adipose tissue accumulation, between COPD and controls. Discrepancies between the present and previous studies as to whether or not COPD is a risk factor for metabolic abnormalities could be related to differences in COPD phenotype or disease severity of the study populations.

Body Composition and COPD: A New Perspective

“… 50 , 57 , 58 The aberrant build up of VAT in COPD patients may worsen airway obstruction by decreasing lung compliance, impairing chest wall or diaphragm movement. 59 …”

“…50,57,58 The aberrant build up of VAT in COPD patients may worsen airway obstruction by decreasing lung compliance, impairing chest wall or diaphragm movement. 59 VAT that has accumulated abnormally has a metabolic activity that results in the production of numerous inflammatory mediators, such as TNF-α, interleukin (IL)-6, leptin, adiponectin, and others. This can support theories about ectopic fat accumulation and a poor prognosis, 60 and the release of inflammatory mediators into the blood brought on by VAT will worsen the condition of COPD patients.…”

Metabolic pathways in immune senescence and inflammaging: Novel therapeutic strategy for chronic inflammatory lung diseases. An EAACI position paper from the Task Force for Immunopharmacology

“…220 A profile of 50 serum lipid metabolites, including phospholipids, sphingolipids, glycerophospholipid, and cholesterol esters, can distinguish COPD from healthy subjects: COPD can be considered a systemic hypometabolic state with reduced levels of N-acetylglycoprotein, lipoprotein, polyunsaturated fatty acid (pUFA), and lactate but with increased levels of diacylglycerols, branched chain amino acids, palmitoleic, oleic and linoleic acids. [221][222][223][224][225][226][227][228] Females with non-severe COPD have less pulmonary emphysema but more small airways disease than males, but this difference disappears as lung function decreases. How sex-related metabotypes may affect airway remodeling is unknown, but there is evidence for sex-related differences in the metabolites lysoPA (16:0) and lysoPA (18:2) in COPD.…”

“…A profile of 50 serum lipid metabolites, including phospholipids, sphingolipids, glycerophospholipid, and cholesterol esters, can distinguish COPD from healthy subjects: COPD can be considered a systemic hypometabolic state with reduced levels of N‐acetyl‐glycoprotein, lipoprotein, polyunsaturated fatty acid (pUFA), and lactate but with increased levels of diacylglycerols, branched chain amino acids, palmitoleic, oleic and linoleic acids 221–228 …”

Skeletal Myosteatosis is Associated with Systemic Inflammation and a Loss of Muscle Bioenergetics in Stable COPD

“…16,21 In contrast, a population-based cohort found no difference in the metabolic phenotype, including VAT, between COPD and controls. 67 These discrepancies between studies, whether COPD is a risk factor for metabolic abnormalities or not, are best explained by differences in COPD phenotype or disease severity of the study populations. Figure 2 summarises the metabolic profile of the COPD cohort studied and the VCGs in the present study.…”