Lung, Fat and Bone: Increased Adiponectin Associates with the Combination of Smoking-Related Lung Disease and Osteoporosis

Chronic Obstr Pulm Dis. 2018 Apr 1;5(2):134-143. doi: 10.15326/jcopdf.5.2.2016.0174.

Abstract

Background: Adiponectin has been proposed as a biomarker of disease severity and progression in chronic obstructive pulmonary disease (COPD) and associated with spirometry-defined COPD and with computed tomography (CT)-measured emphysema. Increased adiponectin plays a role in other diseases including diabetes/metabolic syndrome, cardiovascular disease and osteoporosis. Previous studies of adiponectin and COPD have not assessed the relationship of adiponectin to airway disease in smokers and have not evaluated the effect of other comorbid diseases on the relationship of adiponectin and lung disease. We postulated that adiponectin levels would associate with both airway disease and emphysema in smokers with and without COPD, and further postulated that body composition and the comorbid diseases of osteoporosis, cardiovascular disease and diabetes might influence adiponectin levels. Methods: Current and former smokers from the COPD Genetic Epidemiology study (COPDGene) (n= 424) were assigned to 4 groups based on CT lung characteristics and volumetric Bone Density (vBMD). Emphysema (% low attenuation area at -950) and airway disease (Wall area %) were used to assess smoking-related lung disease (SRLD). Group 1) Normal Lung with Normal vBMD; Group 2) Normal Lung and Osteoporosis; Group 3) SRLD with Normal vBMD; Group 4) SRLD with Osteoporosis. Cardiovascular disease (CVD), diabetes, C-reactive protein (CRP) and T-cadherin (soluble receptor for adiponectin) levels were defined for each group. Body composition was derived from chest CT. Multivariable regression assessed effects of emphysema, wall area %, bone density, comorbid diseases and other key factors on log adiponectin. Results: Group 4, SRLD with Osteoporosis, had significantly higher adiponectin levels compared to other groups and the effect persisted in adjusted models. Systemic inflammation (by CRP) was associated with SRLD in Groups 3 and 4 but not with osteoporosis alone. In regression models, lower bone density and worse emphysema were associated with higher adiponectin. Airway disease was associated with higher adiponectin levels when T-cadherin was added to the model. Male gender, greater muscle and fat were associated with lower adiponectin. Conclusions: Adiponectin is increased with both airway disease and emphysema in smokers. Bone density, and fat and muscle composition are all significant factors predicting adiponectin that should be considered when it is used as a biomarker of COPD. Increased adiponectin from chronic inflammation may play a role in the progression of bone loss in COPD and other lung diseases.

Keywords: C-reactive protein; CDH13; QCT; T cadherin; adiponectin; airway disease; body composition; bone mineral density; copd; emphysema; muscle area; osteoporosis; pectoralis; smoking-related lung disease; subcutaneous fat area; systemic inflammation; visceral fa; volumetric BMD.

Grant support

The project described was supported by Award Number R01HL089897 and Award Number R01HL089856 from the National Heart, Lung, and Blood Institute. It was also supported by 1R01HL122464. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Heart, Lung, and Blood Institute or the National Institutes of Health. The COPDGene® project is also supported by the COPD Foundation through contributions made to an Industry Advisory Board comprised of AstraZeneca, Boehringer Ingelheim, Novartis, Pfizer, Siemens, Sunovion, and GlaxoSmithKline.