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The novel hormone ghrelin has been proposed as a treatment for this condition. Increases in food intake and direct effects on muscle proteolysis and protein synthesis are likely to mediate these effects, but the pathways leading to these events are not well understood.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We characterized molecular pathways involved in muscle atrophy induced by Lewis lung carcinoma (LLC) tumour implantation in c57\/bl6 adult male mice and by administration of the chemotherapeutic agent cisplatin in mice and in C2C12 myotubes. The effects of exogenous ghrelin administration and its mechanisms of action were examined in these settings.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Tumour implantation and cisplatin induced muscle atrophy by activating pro\u2010inflammatory cytokines, p38\u2010C\/EBP\u2010\u03b2, and myostatin, and by down\u2010regulating Akt, myoD, and myogenin, leading to activation of ubiquitin\u2010proteasome\u2010mediated proteolysis and muscle weakness. Tumour implantation also increased mortality.\n                      <jats:italic>In vitro<\/jats:italic>\n                      , cisplatin up\u2010regulated myostatin and atrogin\u20101 by activating C\/EBP\u2010\u03b2 and FoxO1\/3. Ghrelin prevented these changes\n                      <jats:italic>in vivo<\/jats:italic>\n                      and\n                      <jats:italic>in vitro<\/jats:italic>\n                      , significantly increasing muscle mass (\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&lt;\u20090.05 for LLC and\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&lt;\u20090.01 for cisplatin models) and grip strength (\n                      <jats:italic>P<\/jats:italic>\n                      \u2009=\u20090.038 for LLC and\n                      <jats:italic>P<\/jats:italic>\n                      \u2009=\u20090.001 for cisplatin models) and improving survival (\n                      <jats:italic>P<\/jats:italic>\n                      \u2009=\u20090.021 for LLC model).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Ghrelin prevents muscle atrophy by down\u2010regulating inflammation, p38\/C\/EBP\u2010\u03b2\/myostatin, and activating Akt, myogenin, and myoD. These changes appear, at least in part, to target muscle cells directly. Ghrelin administration in this setting is associated with improved muscle strength and survival.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/jcsm.12023","type":"journal-article","created":{"date-parts":[[2015,4,22]],"date-time":"2015-04-22T05:47:09Z","timestamp":1429681629000},"page":"132-143","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":184,"title":["Ghrelin prevents tumour\u2010 and cisplatin\u2010induced muscle wasting: characterization of multiple mechanisms involved"],"prefix":"10.1002","volume":"6","author":[{"given":"Ji\u2010an","family":"Chen","sequence":"first","affiliation":[{"name":"Department of Health Education, College of Preventive Medicine Third Military Medical University  Chongqing China"},{"name":"Division of Endocrinology, Diabetes and Metabolism, MCL, Center for Translational Research on Inflammatory Diseases Michael E. DeBakey Veterans Affairs Medical Center, Department of Medicine, Baylor College of Medicine  Houston TX USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andres","family":"Splenser","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Diabetes and Metabolism, MCL, Center for Translational Research on Inflammatory Diseases Michael E. DeBakey Veterans Affairs Medical Center, Department of Medicine, Baylor College of Medicine  Houston TX USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bobby","family":"Guillory","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Diabetes and Metabolism, MCL, Center for Translational Research on Inflammatory Diseases Michael E. DeBakey Veterans Affairs Medical Center, Department of Medicine, Baylor College of Medicine  Houston TX USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiaohua","family":"Luo","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Diabetes and Metabolism, MCL, Center for Translational Research on Inflammatory Diseases Michael E. DeBakey Veterans Affairs Medical Center, Department of Medicine, Baylor College of Medicine  Houston TX USA"},{"name":"Department of Environmental Hygiene, College of Preventive Medicine Third Military Medical University  Chongqing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Meenal","family":"Mendiratta","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Diabetes and Metabolism, MCL, Center for Translational Research on Inflammatory Diseases Michael E. DeBakey Veterans Affairs Medical Center, Department of Medicine, Baylor College of Medicine  Houston TX USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Blaga","family":"Belinova","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Diabetes and Metabolism, MCL, Center for Translational Research on Inflammatory Diseases Michael E. DeBakey Veterans Affairs Medical Center, Department of Medicine, Baylor College of Medicine  Houston TX USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tripti","family":"Halder","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Diabetes and Metabolism, MCL, Center for Translational Research on Inflammatory Diseases Michael E. 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