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      Cachexia in chronic obstructive pulmonary disease: new insights and therapeutic perspective

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          Abstract

          Cachexia and muscle wasting are well recognized as common and partly reversible features of chronic obstructive pulmonary disease (COPD), adversely affecting disease progression and prognosis. This argues for integration of weight and muscle maintenance in patient care. In this review, recent insights are presented in the diagnosis of muscle wasting in COPD, the pathophysiology of muscle wasting, and putative mechanisms involved in a disturbed energy balance as cachexia driver. We discuss the therapeutic implications of these new insights for optimizing and personalizing management of COPD‐induced cachexia.

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          Satellite cells are essential for skeletal muscle regeneration: the cell on the edge returns centre stage.

          Frédéric Relaix, Peter S. Zammit (2012)
          Following their discovery in 1961, it was speculated that satellite cells were dormant myoblasts, held in reserve until required for skeletal muscle repair. Evidence for this accumulated over the years, until the link between satellite cells and the myoblasts that appear during muscle regeneration was finally established. Subsequently, it was demonstrated that, when grafted, satellite cells could also self-renew, conferring on them the coveted status of 'stem cell'. The emergence of other cell types with myogenic potential, however, questioned the precise role of satellite cells. Here, we review recent recombination-based studies that have furthered our understanding of satellite cell biology. The clear consensus is that skeletal muscle does not regenerate without satellite cells, confirming their pivotal and non-redundant role.
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            Characteristics of physical activities in daily life in chronic obstructive pulmonary disease.

            Fabio Pitta, Thierry Troosters, Martijn Spruit … (2005)
            Quantification of physical activities in daily life in patients with chronic obstructive pulmonary disease has increasing clinical interest. However, detailed comparison with healthy subjects is not available. Furthermore, it is unknown whether time spent actively during daily life is related to lung function, muscle force, or maximal and functional exercise capacity. We assessed physical activities and movement intensity with the DynaPort activity monitor in 50 patients (age 64 +/- 7 years; FEV1 43 +/- 18% predicted) and 25 healthy elderly individuals (age 66 +/- 5 years). Patients showed lower walking time (44 +/- 26 vs. 81 +/- 26 minutes/day), standing time (191 +/- 99 vs. 295 +/- 109 minutes/day), and movement intensity during walking (1.8 +/- 0.3 vs. 2.4 +/- 0.5 m/second2; p < 0.0001 for all), as well as higher sitting time (374 +/- 139 vs. 306 +/- 108 minutes/day; p = 0.04) and lying time (87 +/- 97 vs. 29 +/- 33 minutes/day; p = 0.004). Walking time was highly correlated with the 6-minute walking test (r = 0.76, p < 0.0001) and more modestly to maximal exercise capacity, lung function, and muscle force (0.28 < r < 0.64, p < 0.05). Patients with chronic obstructive pulmonary disease are markedly inactive in daily life. Functional exercise capacity is the strongest correlate of physical activities in daily life.
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              Amino acid sufficiency and mTOR regulate p70 S6 kinase and eIF-4E BP1 through a common effector mechanism.

              C Belham, K Yonezawa, Joseph Avruch … (1998)
              The present study identifies the operation of a signal tranduction pathway in mammalian cells that provides a checkpoint control, linking amino acid sufficiency to the control of peptide chain initiation. Withdrawal of amino acids from the nutrient medium of CHO-IR cells results in a rapid deactivation of p70 S6 kinase and dephosphorylation of eIF-4E BP1, which become unresponsive to all agonists. Readdition of the amino acid mixture quickly restores the phosphorylation and responsiveness of p70 and eIF-4E BP1 to insulin. Increasing the ambient amino acids to twice that usually employed increases basal p70 activity to the maximal level otherwise attained in the presence of insulin and abrogates further stimulation by insulin. Withdrawal of most individual amino acids also inhibits p70, although with differing potency. Amino acid withdrawal from CHO-IR cells does not significantly alter insulin stimulation of tyrosine phosphorylation, phosphotyrosine-associated phosphatidylinositol 3-kinase activity, c-Akt/protein kinase B activity, or mitogen-activated protein kinase activity. The selective inhibition of p70 and eIF-4E BP1 phosphorylation by amino acid withdrawal resembles the response to rapamycin, which prevents p70 reactivation by amino acids, indicating that mTOR is required for the response to amino acids. A p70 deletion mutant, p70Delta2-46/DeltaCT104, that is resistant to inhibition by rapamycin (but sensitive to wortmannin) is also resistant to inhibition by amino acid withdrawal, indicating that amino acid sufficiency and mTOR signal to p70 through a common effector, which could be mTOR itself, or an mTOR-controlled downstream element, such as a protein phosphatase.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Cachexia Sarcopenia Muscle
                Journal ID (iso-abbrev): J Cachexia Sarcopenia Muscle
                Journal ID (doi): 10.1007/13539.2190-6009
                Journal ID (publisher-id): JCSM
                Title: Journal of Cachexia, Sarcopenia and Muscle
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Print): 2190-5991
                ISSN (Electronic): 2190-6009
                Publication date (Electronic): 07 September 2015
                Publication date (Print): March 2016
                Volume: 7
                Issue: 1 ( doiID: 10.1002/jcsm.v7.1 )
                Pages: 5-22
                Affiliations
                [ 1 ] Department of Respiratory MedicineNUTRIM School of Nutrition and Translational Research in Metabolism MaastrichtThe Netherlands
                Author notes
                [*] [* ]Correspondence to: Prof. Dr. A. M. W. J. Schols, Department of Respiratory Medicine, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University Medical Centre, P.O. Box 5800, 6202 AZ Maastricht, The Netherlands: Tel: +31 433875046, Email: a.schols@ 123456maastrichtuniversity.nl
                [†]

                Both authors contributed equally

                Article
                Publisher ID: JCSM12062 Other ID: JCSM-D-15-00018
                DOI: 10.1002/jcsm.12062
                PMC ID: 4799856
                PubMed ID: 27066314
                SO-VID: ac7749d4-9254-4f77-be7c-25b24efeb7ff
                Copyright © © 2015 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by John Wiley & Sons Ltd on behalf of the Society of Sarcopenia, Cachexia and Wasting Disorders
                License:

                This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 18 January 2015
                Date revision received : 05 July 2015
                Date accepted : 12 July 2015
                Page count
                Pages: 18
                Categories
                Subject: Review
                Subject: Reviews
                Custom metadata
                source-schema-version-number 2.0
                component-id jcsm12062
                cover-date March 2016
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_NLMPMC version:4.8.5 mode:remove_FC converted:20.03.2016

                ScienceOpen disciplines: Orthopedics
                Keywords: copd,muscle,emphysema,energy balance,cachexia,lung cancer
                Data availability:
                ScienceOpen disciplines: Orthopedics
                Keywords: copd, muscle, emphysema, energy balance, cachexia, lung cancer

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