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      Women with COPD by biomass show different serum profile of adipokines, incretins, and peptide hormones than smokers

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          Abstract

          Background

          The 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.

          Methods

          Clinical 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 FEV 1% pred with levels of inflammatory mediators in COPD women.

          Results

          FEV1% 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.

          Conclusions

          women 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.

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          Most cited references30

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          Obesity-associated improvements in metabolic profile through expansion of adipose tissue.

          Excess caloric intake can lead to insulin resistance. The underlying reasons are complex but likely related to ectopic lipid deposition in nonadipose tissue. We hypothesized that the inability to appropriately expand subcutaneous adipose tissue may be an underlying reason for insulin resistance and beta cell failure. Mice lacking leptin while overexpressing adiponectin showed normalized glucose and insulin levels and dramatically improved glucose as well as positively affected serum triglyceride levels. Therefore, modestly increasing the levels of circulating full-length adiponectin completely rescued the diabetic phenotype in ob/ob mice. They displayed increased expression of PPARgamma target genes and a reduction in macrophage infiltration in adipose tissue and systemic inflammation. As a result, the transgenic mice were morbidly obese, with significantly higher levels of adipose tissue than their ob/ob littermates, leading to an interesting dichotomy of increased fat mass associated with improvement in insulin sensitivity. Based on these data, we propose that adiponectin acts as a peripheral "starvation" signal promoting the storage of triglycerides preferentially in adipose tissue. As a consequence, reduced triglyceride levels in the liver and muscle convey improved systemic insulin sensitivity. These mice therefore represent what we believe is a novel model of morbid obesity associated with an improved metabolic profile.
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            An official American Thoracic Society public policy statement: Novel risk factors and the global burden of chronic obstructive pulmonary disease.

            Although cigarette smoking is the most important cause of chronic obstructive pulmonary disease (COPD), a substantial proportion of COPD cases cannot be explained by smoking alone. To evaluate the risk factors for COPD besides personal cigarette smoking. We constituted an ad hoc subcommittee of the American Thoracic Society Environmental and Occupational Health Assembly. An international group of members was invited, based on their scientific expertise in a specific risk factor for COPD. For each risk factor area, the committee reviewed the literature, summarized the evidence, and developed conclusions about the likelihood of it causing COPD. All conclusions were based on unanimous consensus. The population-attributable fraction for smoking as a cause of COPD ranged from 9.7 to 97.9%, but was less than 80% in most studies, indicating a substantial burden of disease attributable to nonsmoking risk factors. On the basis of our review, we concluded that specific genetic syndromes and occupational exposures were causally related to the development of COPD. Traffic and other outdoor pollution, secondhand smoke, biomass smoke, and dietary factors are associated with COPD, but sufficient criteria for causation were not met. Chronic asthma and tuberculosis are associated with irreversible loss of lung function, but there remains uncertainty about whether there are important phenotypic differences compared with COPD as it is typically encountered in clinical settings. In public health terms, a substantive burden of COPD is attributable to risk factors other than smoking. To prevent COPD-related disability and mortality, efforts must focus on prevention and cessation of exposure to smoking and these other, less well-recognized risk factors.
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              Systemic inflammation in chronic obstructive pulmonary disease: a population-based study

              Background Elevated circulating levels of several inflammatory biomarkers have been described in selected patient populations with COPD, although less is known about their population-based distribution. The aims of this study were to compare the levels of several systemic biomarkers between stable COPD patients and healthy subjects from a population-based sample, and to assess their distribution according to clinical variables. Methods This is a cross-sectional study design of participants in the EPI-SCAN study (40-80 years of age). Subjects with any other condition associated with an inflammatory process were excluded. COPD was defined as a post-bronchodilator FEV1/FVC < 0.70. The reference group was made of non-COPD subjects without respiratory symptoms, associated diseases or prescription of medication. Subjects were evaluated with quality-of-life questionnaires, spirometry and 6-minute walk tests. Serum C-reactive protein (CRP), tumor necrosis factor (TNF)-α, interleukins (IL-6 and IL-8), alpha1-antitrypsin, fibrinogen, albumin and nitrites/nitrates (NOx) were measured. Results We compared 324 COPD patients and 110 reference subjects. After adjusting for gender, age, BMI and tobacco consumption, COPD patients showed higher levels of CRP (0.477 ± 0.023 vs. 0.376 ± 0.041 log mg/L, p = 0.049), TNF-α (13.12 ± 0.59 vs. 10.47 ± 1.06 pg/mL, p = 0.033), IL-8 (7.56 ± 0.63 vs. 3.57 ± 1.13 pg/ml; p = 0.033) and NOx (1.42 ± 0.01 vs. 1.36 ± 0.02 log nmol/l; p = 0.048) than controls. In COPD patients, serum concentrations of some biomarkers were related to severity and their exercise tolerance was related to serum concentrations of CRP, IL-6, IL-8, fibrinogen and albumin. Conclusions Our results provide population-based evidence that COPD is independently associated with low-grade systemic inflammation, with a different inflammatory pattern than that observed in healthy subjects.
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                Author and article information

                Contributors
                oliveriner@yahoo.com.mx
                mamora572002@yahoo.com.mx
                perezpadilla@gmail.com
                joaquin.zuniga@iner.gob.mx
                mariana.cpriego@gmail.com
                tonatiuhb@gmail.com
                ivettebu@yahoo.com.mx
                yajo19@yahoo.com.mx
                (5255) 54871700 ext. 5257 , carlos.ramos26@yahoo.com.mx
                Journal
                Respir Res
                Respir. Res
                Respiratory Research
                BioMed Central (London )
                1465-9921
                1465-993X
                4 December 2018
                4 December 2018
                2018
                : 19
                : 239
                Affiliations
                [1 ]ISNI 0000 0000 8515 3604, GRID grid.419179.3, Departamento de Investigación en Tabaquismo y EPOC, , Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas (INERICV), ; Ciudad de México, Mexico
                [2 ]ISNI 0000 0000 8515 3604, GRID grid.419179.3, Departamento de Investigación en Fibrosis Pulmonar, , Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas (INERICV), ; Talpan 4502, C.P. 14080 Ciudad de México, Mexico
                [3 ]ISNI 0000 0000 8515 3604, GRID grid.419179.3, Laboratorio de Inmunobiología y Genética, , Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas (INERICV), ; Ciudad de México, Mexico
                [4 ]ISNI 0000 0004 1773 4764, GRID grid.415771.1, Centro de Investigación en Salud Poblacional, Instituto Nacional de Salud Pública (INSP), ; Cuernavaca, Morelos Mexico
                [5 ]ISNI 0000 0001 2157 0393, GRID grid.7220.7, Doctorado en Ciencias Biológicas y de la Salud, , Universidad Autónoma Metropolitana-Xochimilco (UAMX), ; Ciudad de México, Mexico
                Author information
                http://orcid.org/0000-0001-7378-6575
                Article
                943
                10.1186/s12931-018-0943-4
                6280373
                30514305
                a544a11e-3eec-44e5-ab70-2f1efbd3f86f
                © The Author(s). 2018

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 9 August 2018
                : 19 November 2018
                Funding
                Funded by: CONACyT
                Award ID: SALUD-2016-1-272301
                Categories
                Research
                Custom metadata
                © The Author(s) 2018

                Respiratory medicine
                adipokines,biomass smoke exposure,copd,incretins,insulin,peptide hormones,tobacco smoking

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