The exerkine apelin reverses age-associated sarcopenia
Sarcopenia, the degenerative loss of skeletal muscle mass, quality and strength, lacks early diagnostic tools and new therapeutic strategies to prevent the frailty-to-disability transition often responsible for the medical institutionalization of elderly individuals. Herein we report that production...
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| Published in: | Nature Medicine Vol. 24; no. 9; pp. 1360 - 1371 |
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| Main Authors: | , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format: | Journal Article Magazine Article |
| Language: | English |
| Published: |
New York
Nature Publishing Group US
01.09.2018
Nature Publishing Group |
| Subjects: | |
| ISSN: | 1078-8956, 1546-170X, 1546-170X, 1744-7933 |
| Online Access: | Get full text |
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| Abstract | Sarcopenia, the degenerative loss of skeletal muscle mass, quality and strength, lacks early diagnostic tools and new therapeutic strategies to prevent the frailty-to-disability transition often responsible for the medical institutionalization of elderly individuals. Herein we report that production of the endogenous peptide apelin, induced by muscle contraction, is reduced in an age-dependent manner in humans and rodents and is positively associated with the beneficial effects of exercise in older persons. Mice deficient in either apelin or its receptor (APLNR) presented dramatic alterations in muscle function with increasing age. Various strategies that restored apelin signaling during aging further demonstrated that this peptide considerably enhanced muscle function by triggering mitochondriogenesis, autophagy and anti-inflammatory pathways in myofibers as well as enhancing the regenerative capacity by targeting muscle stem cells. Taken together, these findings revealed positive regulatory feedback between physical activity, apelin and muscle function and identified apelin both as a tool for diagnosis of early sarcopenia and as the target of an innovative pharmacological strategy to prevent age-associated muscle weakness and restore physical autonomy.
The muscle-secreted, exercise-induced peptide hormone apelin decreases with aging and sarcopenia, and its repletion in aged mice with recombinant protein improves muscle mass and function. |
|---|---|
| AbstractList | Sarcopenia, the degenerative loss of skeletal muscle mass, quality and strength, lacks early diagnostic tools and new therapeutic strategies to prevent the frailty-to-disability transition often responsible for the medical institutionalization of elderly individuals. Herein we report that production of the endogenous peptide apelin, induced by muscle contraction, is reduced in an age-dependent manner in humans and rodents and is positively associated with the beneficial effects of exercise in older persons. Mice deficient in either apelin or its receptor (APLNR) presented dramatic alterations in muscle function with increasing age. Various strategies that restored apelin signaling during aging further demonstrated that this peptide considerably enhanced muscle function by triggering mitochondriogenesis, autophagy and anti-inflammatory pathways in myofibers as well as enhancing the regenerative capacity by targeting muscle stem cells. Taken together, these findings revealed positive regulatory feedback between physical activity, apelin and muscle function and identified apelin both as a tool for diagnosis of early sarcopenia and as the target of an innovative pharmacological strategy to prevent age-associated muscle weakness and restore physical autonomy. Sarcopenia, the degenerative loss of skeletal muscle mass, quality and strength, lacks early diagnostic tools and new therapeutic strategies to prevent the frailty-to-disability transition often responsible for the medical institutionalization of elderly individuals. Herein we report that production of the endogenous peptide apelin, induced by muscle contraction, is reduced in an age-dependent manner in humans and rodents and is positively associated with the beneficial effects of exercise in older persons. Mice deficient in either apelin or its receptor (APLNR) presented dramatic alterations in muscle function with increasing age. Various strategies that restored apelin signaling during aging further demonstrated that this peptide considerably enhanced muscle function by triggering mitochondriogenesis, autophagy and anti-inflammatory pathways in myofibers as well as enhancing the regenerative capacity by targeting muscle stem cells. Taken together, these findings revealed positive regulatory feedback between physical activity, apelin and muscle function and identified apelin both as a tool for diagnosis of early sarcopenia and as the target of an innovative pharmacological strategy to prevent age-associated muscle weakness and restore physical autonomy.Sarcopenia, the degenerative loss of skeletal muscle mass, quality and strength, lacks early diagnostic tools and new therapeutic strategies to prevent the frailty-to-disability transition often responsible for the medical institutionalization of elderly individuals. Herein we report that production of the endogenous peptide apelin, induced by muscle contraction, is reduced in an age-dependent manner in humans and rodents and is positively associated with the beneficial effects of exercise in older persons. Mice deficient in either apelin or its receptor (APLNR) presented dramatic alterations in muscle function with increasing age. Various strategies that restored apelin signaling during aging further demonstrated that this peptide considerably enhanced muscle function by triggering mitochondriogenesis, autophagy and anti-inflammatory pathways in myofibers as well as enhancing the regenerative capacity by targeting muscle stem cells. Taken together, these findings revealed positive regulatory feedback between physical activity, apelin and muscle function and identified apelin both as a tool for diagnosis of early sarcopenia and as the target of an innovative pharmacological strategy to prevent age-associated muscle weakness and restore physical autonomy. Sarcopenia, the degenerative loss of skeletal muscle mass, quality and strength, lacks early diagnostic tools and new therapeutic strategies to prevent the frailty-to-disability transition often responsible for the medical institutionalization of elderly individuals. Herein we report that production of the endogenous peptide apelin, induced by muscle contraction, is reduced in an age-dependent manner in humans and rodents and is positively associated with the beneficial effects of exercise in older persons. Mice deficient in either apelin or its receptor (APLNR) presented dramatic alterations in muscle function with increasing age. Various strategies that restored apelin signaling during aging further demonstrated that this peptide considerably enhanced muscle function by triggering mitochondriogenesis, autophagy and anti-inflammatory pathways in myofibers as well as enhancing the regenerative capacity by targeting muscle stem cells. Taken together, these findings revealed positive regulatory feedback between physical activity, apelin and muscle function and identified apelin both as a tool for diagnosis of early sarcopenia and as the target of an innovative pharmacological strategy to prevent age-associated muscle weakness and restore physical autonomy. The muscle-secreted, exercise-induced peptide hormone apelin decreases with aging and sarcopenia, and its repletion in aged mice with recombinant protein improves muscle mass and function. Sarcopenia, the degenerative loss of skeletal muscle mass, quality and strength, lacks early diagnostic tools and new therapeutic strategies to prevent the frailty-to-disability transition often responsible for the medical institutionalization of elderly individuals. Herein we report that production of the endogenous peptide apelin, induced by muscle contraction, is reduced in an age-dependent manner in humans and rodents and is positively associated with the beneficial effects of exercise in older persons. Mice deficient in either apelin or its receptor (APLNR) presented dramatic alterations in muscle function with increasing age. Various strategies that restored apelin signaling during aging further demonstrated that this peptide considerably enhanced muscle function by triggering mitochondriogenesis, autophagy and anti-inflammatory pathways in myofibers as well as enhancing the regenerative capacity by targeting muscle stem cells. Taken together, these findings revealed positive regulatory feedback between physical activity, apelin and muscle function and identified apelin both as a tool for diagnosis of early sarcopenia and as the target of an innovative pharmacological strategy to prevent age-associated muscle weakness and restore physical autonomy. The muscle-secreted, exercise-induced peptide hormone apelin decreases with aging and sarcopenia, and its repletion in aged mice with recombinant protein improves muscle mass and function. |
| Audience | Academic |
| Author | Batut, Aurelie Chopard, Angèle Camus, Mylène Dray, Cedric Geoffre, Nancy Dortignac, Alizée Pagano, Allan F. Lukjanenko, Laura Pillard, Fabien Vinel, Claire Pahor, Marco Chaoui, Karima Karaz, Sonia Pradère, Jean-Philippe Vellas, Bruno Valet, Philippe Deleruyelle, Simon Mouisel, Etienne Pereira, Ophelie Vigneau, Mathieu Burlet-Schiltz, Odile Feige, Jerome N. Lee, Umji Le Gonidec, Sophie Guyonnet, Sophie Bigot, Anne Cesari, Matteo Mouly, Vincent |
| Author_xml | – sequence: 1 givenname: Claire surname: Vinel fullname: Vinel, Claire organization: Institut des Maladies Métaboliques et Cardiovasculaires, INSERM U1048, Université de Toulouse, Université Paul Sabatier – sequence: 2 givenname: Laura surname: Lukjanenko fullname: Lukjanenko, Laura organization: Aging Department, Nestlé Institute of Health Sciences SA, Ecole Polytechnique Fédérale de Lausanne Innovation Park – sequence: 3 givenname: Aurelie surname: Batut fullname: Batut, Aurelie organization: Institut des Maladies Métaboliques et Cardiovasculaires, INSERM U1048, Université de Toulouse, Université Paul Sabatier – sequence: 4 givenname: Simon surname: Deleruyelle fullname: Deleruyelle, Simon organization: Institut des Maladies Métaboliques et Cardiovasculaires, INSERM U1048, Université de Toulouse, Université Paul Sabatier – sequence: 5 givenname: Jean-Philippe surname: Pradère fullname: Pradère, Jean-Philippe organization: Institut des Maladies Métaboliques et Cardiovasculaires, INSERM U1048, Université de Toulouse, Université Paul Sabatier – sequence: 6 givenname: Sophie surname: Le Gonidec fullname: Le Gonidec, Sophie organization: Institut des Maladies Métaboliques et Cardiovasculaires, INSERM U1048, Université de Toulouse, Université Paul Sabatier – sequence: 7 givenname: Alizée surname: Dortignac fullname: Dortignac, Alizée organization: Institut des Maladies Métaboliques et Cardiovasculaires, INSERM U1048, Université de Toulouse, Université Paul Sabatier – sequence: 8 givenname: Nancy surname: Geoffre fullname: Geoffre, Nancy organization: Institut des Maladies Métaboliques et Cardiovasculaires, INSERM U1048, Université de Toulouse, Université Paul Sabatier – sequence: 9 givenname: Ophelie surname: Pereira fullname: Pereira, Ophelie organization: Institut des Maladies Métaboliques et Cardiovasculaires, INSERM U1048, Université de Toulouse, Université Paul Sabatier – sequence: 10 givenname: Sonia surname: Karaz fullname: Karaz, Sonia organization: Aging Department, Nestlé Institute of Health Sciences SA, Ecole Polytechnique Fédérale de Lausanne Innovation Park – sequence: 11 givenname: Umji surname: Lee fullname: Lee, Umji organization: Aging Department, Nestlé Institute of Health Sciences SA, Ecole Polytechnique Fédérale de Lausanne Innovation Park – sequence: 12 givenname: Mylène surname: Camus fullname: Camus, Mylène organization: Institut de Pharmacologie et de Biologie Structurale–CNRS, Université de Toulouse, Université Paul Sabatier – sequence: 13 givenname: Karima surname: Chaoui fullname: Chaoui, Karima organization: Institut de Pharmacologie et de Biologie Structurale–CNRS, Université de Toulouse, Université Paul Sabatier – sequence: 14 givenname: Etienne surname: Mouisel fullname: Mouisel, Etienne organization: Institut des Maladies Métaboliques et Cardiovasculaires, INSERM U1048, Université de Toulouse, Université Paul Sabatier – sequence: 15 givenname: Anne surname: Bigot fullname: Bigot, Anne organization: Institut de Myologie, Université Pierre et Marie Curie, Paris 6 UM76, Univ. Paris 6/U974, UMR7215, CNRS, Pitié-Salpétrière–INSERM, UMRS 974 – sequence: 16 givenname: Vincent surname: Mouly fullname: Mouly, Vincent organization: Institut de Myologie, Université Pierre et Marie Curie, Paris 6 UM76, Univ. Paris 6/U974, UMR7215, CNRS, Pitié-Salpétrière–INSERM, UMRS 974 – sequence: 17 givenname: Mathieu surname: Vigneau fullname: Vigneau, Mathieu organization: Institut des Technologies Avancées en Science du Vivant–USR3505 Centre Pierre Potier – sequence: 18 givenname: Allan F. surname: Pagano fullname: Pagano, Allan F. organization: Université de Montpellier, Institut National de la Recherche Agronomique, UMR866 Dynamique Musculaire et Métabolisme – sequence: 19 givenname: Angèle surname: Chopard fullname: Chopard, Angèle organization: Université de Montpellier, Institut National de la Recherche Agronomique, UMR866 Dynamique Musculaire et Métabolisme – sequence: 20 givenname: Fabien surname: Pillard fullname: Pillard, Fabien organization: Institut des Maladies Métaboliques et Cardiovasculaires, INSERM U1048, Université de Toulouse, Université Paul Sabatier – sequence: 21 givenname: Sophie surname: Guyonnet fullname: Guyonnet, Sophie organization: Gérontopole Toulouse-Purpan UMR 1027 – sequence: 22 givenname: Matteo surname: Cesari fullname: Cesari, Matteo organization: Gérontopole Toulouse-Purpan UMR 1027 – sequence: 23 givenname: Odile surname: Burlet-Schiltz fullname: Burlet-Schiltz, Odile organization: Institut de Pharmacologie et de Biologie Structurale–CNRS, Université de Toulouse, Université Paul Sabatier – sequence: 24 givenname: Marco surname: Pahor fullname: Pahor, Marco organization: Institute on Aging, College of Medicine, University of Florida – sequence: 25 givenname: Jerome N. surname: Feige fullname: Feige, Jerome N. organization: Aging Department, Nestlé Institute of Health Sciences SA, Ecole Polytechnique Fédérale de Lausanne Innovation Park – sequence: 26 givenname: Bruno surname: Vellas fullname: Vellas, Bruno organization: Gérontopole Toulouse-Purpan UMR 1027 – sequence: 27 givenname: Philippe surname: Valet fullname: Valet, Philippe organization: Institut des Maladies Métaboliques et Cardiovasculaires, INSERM U1048, Université de Toulouse, Université Paul Sabatier – sequence: 28 givenname: Cedric surname: Dray fullname: Dray, Cedric email: cedric.dray@inserm.fr organization: Institut des Maladies Métaboliques et Cardiovasculaires, INSERM U1048, Université de Toulouse, Université Paul Sabatier |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30061698$$D View this record in MEDLINE/PubMed https://hal.science/hal-01918096$$DView record in HAL |
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| Title | The exerkine apelin reverses age-associated sarcopenia |
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