Ectopic adiposity and cardiometabolic health in COPD

Abstract

Rationale

Obesity/overweight is the most prevalent body composition abnormality in COPD. However, little is known about the impact of fat distribution on cardiometabolic health in COPD.

Objective

To study the associations between ectopic adiposity, cardiometabolic health, and COPD.

Methods

A total of 263 subjects (166 males; age=65±9 years) were randomly selected from the general population. Subjects were classified as non-COPD controls and COPD, according to the Global initiative for chronic Obstructive Lung Disease (GOLD) classification, and the presence of cardiometabolic comorbidities was recorded. Ectopic fat accumulation was documented from computed tomography measurements of visceral adipose tissue cross-sectional areas and muscle mean attenuation, assessed at L4–L5. Blood glucose, lipid, and adipokine profiles were also evaluated.

Results

After correcting for age, sex, and tobacco exposure, visceral adipose tissue cross-sectional area was higher in GOLD 2+ compared to GOLD 1 individuals. Consistent with this, mean muscle tissue attenuation was lower in GOLD 2+ vs GOLD 1 and non-COPD controls (P<0.001). In multiple regression models, visceral adipose tissue cross-sectional area was strongly associated with hypertension (P<0.001) and diabetes (P<0.001), while muscle attenuation was associated with coronary artery disease (P<0.001). Blood glucose, lipid, and adipokine profiles were similar across groups with the exception of leptin level which was higher in GOLD 2+ subjects compared to GOLD 1 and controls.

Conclusion

GOLD 2+ COPD was associated with ectopic fat accumulation which modulated cardiometabolic health.

Keywords:

• chronic obstructive pulmonary disease
• obesity
• abdominal
• comorbidity
• ectopic adiposity
• cardiometabolic health

Acknowledgments

The authors thank Cynthia Brouillard (Institut Universitaire de Cardiologie et de Pneumologie de Québec, QC, Canada), Palmina Mancino, David Latreille, Jacinthe Baril, Laura Labonté (Research Institute of the McGill University Health Center, Montreal, QC, Canada) who were responsible for the clinical evaluation of study participants, Véronic Tremblay from the body composition analysis platform of the Institut Universitaire de cardiologie et de pneumologie de Québec for ensuring standardization of the CT images analyses, Nathalie Mercier and Karine Bibeau for quantifying coronary artery calcifications, Sylvain Pouliot who analyzed the metabolic and adipokine profiles, and Gaétan Daigle for statistical assistance. They also thank all the subjects, investigators, and study site staff who participated in CanCOLD.

The Canadian Cohort Obstructive Lung Disease (Can-COLD) study is currently funded by the Canadian Respiratory Research Network (industry partners: Astra Zeneca Canada Ltd., Boehringer Ingelheim Canada Ltd., GlaxoSmithKline Canada Ltd., and Novartis). Previous funding partners were the CIHR (CIHR/Rx&D Collaborative Research Program Operating Grants-93326) and the Respiratory Health Network of the FRSQ (industry partners: Almirall, Merck Nycomed, Pfizer Canada Ltd., and Thera technologies). J-PD is the scientific director of the International Chair on Cardio-metabolic Risk which is based at the Faculty of medicine, Université Laval. EL is a research scholar from the Fonds de Recherche Québec – Santé (FRQS). JB holds a GSK/CIHR Research Chair on COPD at McGill University. FM holds a GSK/CIHR Research Chair on COPD at Université Laval.

Disclosure

The authors report no conflicts of interest in this work.