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      Highlights from the 7th Cachexia Conference: muscle wasting pathophysiological detection and novel treatment strategies

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          Abstract

          This article highlights preclinical and clinical studies in the field of wasting disorders that were presented at the 7th Cachexia Conference held in Kobe, Japan, in December 2013. This year, the main topics were the development of new methods and new biomarkers in the field of cachexia and wasting disorders with particular focus on inflammatory pathways, growth differentiation factor-15, myostatin, the ubiquitin proteasome-dependent pathway, valosin and the regulation of ubiquitin-specific protease 19 that is involved in the differentiation of myogenin and myosin heavy chain. This article presents highlights from the development of drugs that have shown potential in the treatment of wasting disorders, particularly the ghrelin receptor agonist anamorelin, the myostatin antagonist REGN1033, the selective androgen receptor modulators enobosarm and TEI-E0001, and the anabolic catabolic transforming agent espindolol. In addition, novel data on the prevalence and detection methods of muscle wasting/sarcopenia are presented, including the D3-creatine dilution method and several new biomarkers.

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          Most cited references 15

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          Cachexia: a new definition.

          On December 13th and 14th a group of scientists and clinicians met in Washington, DC, for the cachexia consensus conference. At the present time, there is no widely agreed upon operational definition of cachexia. The lack of a definition accepted by clinician and researchers has limited identification and treatment of cachectic patient as well as the development and approval of potential therapeutic agents. The definition that emerged is: "cachexia, is a complex metabolic syndrome associated with underlying illness and characterized by loss of muscle with or without loss of fat mass. The prominent clinical feature of cachexia is weight loss in adults (corrected for fluid retention) or growth failure in children (excluding endocrine disorders). Anorexia, inflammation, insulin resistance and increased muscle protein breakdown are frequently associated with cachexia. Cachexia is distinct from starvation, age-related loss of muscle mass, primary depression, malabsorption and hyperthyroidism and is associated with increased morbidity. While this definition has not been tested in epidemiological or intervention studies, a consensus operational definition provides an opportunity for increased research.
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            Mitochondrial dysfunction and sarcopenia of aging: from signaling pathways to clinical trials.

            Sarcopenia, the age-related loss of muscle mass and function, imposes a dramatic burden on individuals and society. The development of preventive and therapeutic strategies against sarcopenia is therefore perceived as an urgent need by health professionals and has instigated intensive research on the pathophysiology of this syndrome. The pathogenesis of sarcopenia is multifaceted and encompasses lifestyle habits, systemic factors (e.g., chronic inflammation and hormonal alterations), local environment perturbations (e.g., vascular dysfunction), and intramuscular specific processes. In this scenario, derangements in skeletal myocyte mitochondrial function are recognized as major factors contributing to the age-dependent muscle degeneration. In this review, we summarize prominent findings and controversial issues on the contribution of specific mitochondrial processes - including oxidative stress, quality control mechanisms and apoptotic signaling - on the development of sarcopenia. Extramuscular alterations accompanying the aging process with a potential impact on myocyte mitochondrial function are also discussed. We conclude with presenting methodological and safety considerations for the design of clinical trials targeting mitochondrial dysfunction to treat sarcopenia. Special emphasis is placed on the importance of monitoring the effects of an intervention on muscle mitochondrial function and identifying the optimal target population for the trial. This article is part of a Directed Issue entitled: Molecular basis of muscle wasting. Copyright © 2013 Elsevier Ltd. All rights reserved.
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              Muscle wasting in patients with chronic heart failure: results from the studies investigating co-morbidities aggravating heart failure (SICA-HF).

              To assess the prevalence and clinical impact of reductions in the skeletal muscle mass of patients with chronic heart failure (HF). Chronic HF is accompanied by co-morbidities that influence the quality of life and outcomes. We prospectively enrolled 200 patients with chronic HF. The appendicular skeletal muscle mass of the arms and the legs combined, was assessed by dual energy X-ray absorptiometry. We analysed the muscle strength in arms and legs, and all patients underwent a 6-min walk test, a 4-m walk test, and spiroergometry testing. Muscle wasting was defined as the appendicular muscle mass 2 SD below the mean of a healthy reference group of adults aged 18-40 years, as suggested for the diagnosis of muscle wasting in healthy ageing (sarcopenia). Muscle wasting was detected in 39 (19.5%) subjects. Patients with muscle wasting had significantly lower values for handgrip and quadriceps strength as well as lower total peak oxygen consumption (peakVO2, 1173 ± 433 vs. 1622 ± 456 mL/min), lower exercise time (7.7 ± 3.8 vs. 10.22 ± 3.0 min, both P < 0.001), and lower left ventricular ejection fraction (LVEF, P = 0.05) than patients without. The distance walked during 6 min and the gait speed during the 4-m walk were lower in patients with muscle wasting (both P < 0.05). Serum levels of interleukin-6 were significantly elevated in patients with muscle wasting (P = 0.001). Logistic regression showed muscle wasting to be independently associated with reduced peak VO2 adjusted for age, sex, New York Heart Association class, haemoglobin, LVEF, distance walked in 6 minutes, and the number of co-morbidities (odds ratio 6.53, p = 0.01). Muscle wasting is a frequent co-morbidity among patients with chronic HF. Patients with muscle wasting present with reduced exercise capacity and muscle strength, and advanced disease.
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                Author and article information

                Contributors
                +49-30-450553506 , +49-30-4507553506 , stephan.von.haehling@web.de
                Journal
                J Cachexia Sarcopenia Muscle
                J Cachexia Sarcopenia Muscle
                Journal of Cachexia, Sarcopenia and Muscle
                Springer Berlin Heidelberg (Berlin/Heidelberg )
                2190-5991
                2190-6009
                5 March 2014
                March 2014
                : 5
                : 1
                : 27-34
                Affiliations
                [ ]Applied Cachexia Research, Department of Cardiology, Charité Medical School, Campus Virchow-Klinikum, Augustenburger Platz 1, 13353 Berlin, Germany
                [ ]Centre for Stroke Research Berlin, Charité Medical School, Berlin, Germany
                Article
                136
                10.1007/s13539-014-0136-z
                3953317
                24595460
                © Springer-Verlag Berlin Heidelberg 2014
                Categories
                Meeting Report
                Custom metadata
                © Springer-Verlag Berlin Heidelberg 2014

                Orthopedics

                therapy, cachexia, muscle  wasting, sarcopenia

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