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      Increased serum levels of S100A1, ZAG, and adiponectin in cachectic patients with COPD

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          COPD is a common irreversible obstructive airway disease. S100A1, ZAG, and adiponectin are important regulators of energy metabolism and body weight. Therefore, the aim of this study was to assess resting metabolic rate (RMR) and its association with serum levels of S100A1, ZAG, and adiponectin in cachectic and noncachectic COPD patients.

          Patients and methods

          Ninety men with COPD, aged 40–70 years, were enrolled in the study. Patients were divided into the following two groups based on the unintentional weight loss of .7.5% in previous 6 months: noncachectic (n=45) and cachectic (n=45). The groups were matched based on age and body mass index (BMI). RMR was measured by indirect calorimetry method. Anthropometric indices and body composition were also measured. Serum levels of S100A1, ZAG, and adiponectin were measured by ELISA.


          Cachectic patients had significantly higher RMR than controls ( P<0.001). Serum levels of ZAG, S100A1, and adiponectin were significantly higher in the cachexia group ( P<0.0001). RMR was not significantly associated with S100A1, ZAG, and adiponectin levels. However, weight loss of patients was significantly associated with serum levels of ZAG and adiponectin (both, β=0.22, P=0.03). Strong and positive association were found between the serum levels of S100A1 and ZAG (β=0.88, P<0.0001), S100A1 and adiponectin (β=0.86, P<0.0001), and also ZAG and adiponectin (β=0.83, P<0.0001).


          The potential role of these factors in the wasting process is considerable. Also, the association between serum levels of S100A1, ZAG, and adiponectin represents that these three proteins are probably related to specific functions.

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          Most cited references 34

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          Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease (GOLD) Workshop summary.

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            Mortality in COPD: Role of comorbidities.

            Chronic obstructive pulmonary disease (COPD) represents an increasing burden throughout the world. COPD-related mortality is probably underestimated because of the difficulties associated with identifying the precise cause of death. Respiratory failure is considered the major cause of death in advanced COPD. Comorbidities such as cardiovascular disease and lung cancer are also major causes and, in mild-to-moderate COPD, are the leading causes of mortality. The links between COPD and these conditions are not fully understood. However, a link through the inflammation pathway has been suggested, as persistent low-grade pulmonary and systemic inflammation, both known risk factors for cardiovascular disease and cancer, are present in COPD independent of cigarette smoking. Lung-specific measurements, such as forced expiratory volume in one second (FEV(1)), predict mortality in COPD and in the general population. However, composite tools, such as health-status measurements (e.g. St George's Respiratory Questionnaire) and the BODE index, which incorporates Body mass index, lung function (airflow Obstruction), Dyspnoea and Exercise capacity, predict mortality better than FEV(1) alone. These multidimensional tools may be more valuable because, unlike predictive approaches based on single parameters, they can reflect the range of comorbidities and the complexity of underlying mechanisms associated with COPD. The current paper reviews the role of comorbidities in chronic obstructive pulmonary disease mortality, the putative underlying pathogenic link between chronic obstructive pulmonary disease and comorbid conditions (i.e. inflammation), and the tools used to predict chronic obstructive pulmonary disease mortality.
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              S100 proteins in mouse and man: from evolution to function and pathology (including an update of the nomenclature).

              The S100 protein family is the largest subgroup within the superfamily of proteins carrying the Ca2+-binding EF-hand motif. Despite their small molecular size and their conserved functional domain of two distinct EF-hands, S100 proteins developed a plethora of tissue-specific intra- and extracellular functions. Accordingly, various diseases such as cardiomyopathies, neurodegenerative and inflammatory disorders, and cancer are associated with altered S100 protein levels. Here, we review the different S100 protein functions and related diseases from an evolutionary point of view. We analyzed the structural variations, which are the basis of functional diversification, as well as the genomic organization of the S100 family in human and compared it with the S100 repertoires in mouse and rat. S100 genes and proteins are highly conserved between the different mammalian species. Moreover, we identified evolutionary related subgroups of S100 proteins within the three species, which share functional similarity and form subclusters on the genomic level. The available S100-specific mouse models are summarized and the consequences of our results are discussed with regard to the use of genetically engineered mice as human disease models. An update of the S100 nomenclature is included, because some of the recently identified S100 genes and pseudogenes had to be renamed. Copyright 2004 Elsevier Inc.

                Author and article information

                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                International Journal of COPD
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove Medical Press
                08 October 2018
                : 13
                : 3157-3163
                [1 ]Department of Community Nutrition, Faculty of Nutrition and Food Science, Tabriz University of Medical Sciences, Tabriz, Iran, kheirouris@
                [2 ]Tuberculosis and Lung Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
                Author notes
                Correspondence: Sorayya Kheirouri, Department of Community Nutrition, Faculty of Nutrition and Food Science, Tabriz University of Medical Sciences, Tabriz, Iran, Tel +98 93 5552 1561, Fax +98 41 4225 7858, Email kheirouris@
                © 2018 Mokari-Yamchi et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                Original Research

                Respiratory medicine

                adiponectin, zag, s100a1, rmr, cachexia, copd


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