Abstract

BackgroundThe main causes of COPD are tobacco smoking (COPD-TS) and biomass smoke exposure (COPD-BS). COPD-TS is known to induce changes in adipokines, incretins, and peptide hormones, frequent biomarkers of inflammation; however, it is unknown if similar changes occur in COPD-BS.MethodsClinical and physiological characteristics, and serum concentration of C-peptide, ghrelin, GIP, GLP-1, glucagon, insulin, leptin, PAI-1, resistin, and visfatin were measured in women with COPD-BS, COPD-TS, and healthy controls.Data were compared with one-way ANOVA and Tukey’s post hoc test; nonparametric were expressed as median (interquartile ranges), with Kruskal-Wallis and Dunn’s post-hoc test. Multivariate analysis, age, BMI, MS, and FEV1% pred with levels of inflammatory mediators in COPD women.ResultsFEV1% pred, FVC% pred, and FEV1/FVC ratio were decremented in COPD. In COPD-TS increased C-peptide, ghrelin, GIP, GLP-1, and leptin, and reduced glucagon, PAI-1, resistin, and visfatin. In COPD-BS enlarged ghrelin, insulin, leptin, and PAI-1 comparatively with COPD-TS and control, while C-peptide and GLP-1 relatively with controls; conversely, glucagon, and resistin were reduced. Multivariate analysis showed association of ghrelin, insulin, PAI-1, and visfatin with BS exposure.Conclusionswomen with COPD-BS have a distinct profile of adipokines, incretins, and peptide hormones, and specifically with ghrelin, insulin, PAI-1, and visfatin related to BS exposure.

Highlights

  • The main causes of Chronic obstructive pulmonary disease (COPD) are tobacco smoking (COPD-Tobacco smoking (TS)) and biomass smoke exposure (COPD-BS)

  • COPD associated with BS (COPD-BS) has remarkable pathophysiological differences compared to COPD associated with tobacco smoking (COPD-TS) [3, 4]

  • C-reactive protein (CRP) was elevated in both COPD groups compared to controls; serum glucose was higher in COPD-BS compared with COPD are tobacco smoking (COPD-TS) and controls (Table 1)

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Summary

Introduction

The main causes of COPD are tobacco smoking (COPD-TS) and biomass smoke exposure (COPD-BS). Chronic obstructive pulmonary disease (COPD) is an important cause of global mortality. Tobacco smoking (TS) is the primary cause of COPD, yet, chronic exposure to biomass smoke (BS), mainly wood smoke, is the second risk factor [1]. The clinical profile of COPD associated with BS (COPD-BS) exposure, and its prognostic factors. 7], yet, they rarely present severe airflow obstruction, low diffusing capacity or lung emphysema, which are common features of COPD-TS [8]. Given these differences, it is reasonable to assume that COPD-BS and COPD-TS could express different patterns of metabolic biomarkers. Pre-existing and incident T2DM have been associated with worse outcomes in COPD-TS [9]

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