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Molecular Mechanism Contributing to Malnutrition and Sarcopenia in Patients with Liver Cirrhosis

Liver cirrhosis is frequently accompanied by disease-related malnutrition (DRM) and sarcopenia, defined as loss of skeletal muscle mass and function. DRM and sarcopenia often coexist in cirrhotic patients and are associated with increased morbidity and mortality. The clinical manifestation of both c...

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Autores principales: Meyer, Fatuma, Bannert, Karen, Wiese, Mats, Esau, Susanne, Sautter, Lea F., Ehlers, Luise, Aghdassi, Ali A., Metges, Cornelia C., Garbe, Leif-A., Jaster, Robert, Lerch, Markus M., Lamprecht, Georg, Valentini, Luzia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7432938/
https://www.ncbi.nlm.nih.gov/pubmed/32731496
http://dx.doi.org/10.3390/ijms21155357
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author Meyer, Fatuma
Bannert, Karen
Wiese, Mats
Esau, Susanne
Sautter, Lea F.
Ehlers, Luise
Aghdassi, Ali A.
Metges, Cornelia C.
Garbe, Leif-A.
Jaster, Robert
Lerch, Markus M.
Lamprecht, Georg
Valentini, Luzia
author_facet Meyer, Fatuma
Bannert, Karen
Wiese, Mats
Esau, Susanne
Sautter, Lea F.
Ehlers, Luise
Aghdassi, Ali A.
Metges, Cornelia C.
Garbe, Leif-A.
Jaster, Robert
Lerch, Markus M.
Lamprecht, Georg
Valentini, Luzia
author_sort Meyer, Fatuma
collection PubMed
description Liver cirrhosis is frequently accompanied by disease-related malnutrition (DRM) and sarcopenia, defined as loss of skeletal muscle mass and function. DRM and sarcopenia often coexist in cirrhotic patients and are associated with increased morbidity and mortality. The clinical manifestation of both comorbidities are triggered by multifactorial mechanisms including reduced nutrient and energy intake caused by dietary restrictions, anorexia, neuroendocrine deregulation, olfactory and gustatory deficits. Maldigestion and malabsorption due to small intestinal bacterial overgrowth, pancreatic insufficiency or cholestasis may also contribute to DRM and sarcopenia. Decreased protein synthesis and increased protein degradation is the cornerstone mechanism to muscle loss, among others mediated by disease- and inflammation-mediated metabolic changes, hyperammonemia, increased myostatin and reduced human growth hormone. The concise pathophysiological mechanisms and interactions of DRM and sarcopenia in liver cirrhosis are not completely understood. Furthermore, most knowledge in this field are based on experimental models, but only few data in humans exist. This review summarizes known and proposed molecular mechanisms contributing to malnutrition and sarcopenia in liver cirrhosis and highlights remaining knowledge gaps. Since, in the prevention and treatment of DRM and sarcopenia in cirrhotic patients, more research is needed to identify potential biomarkers for diagnosis and development of targeted therapeutic strategies.
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spelling pubmed-74329382020-08-28 Molecular Mechanism Contributing to Malnutrition and Sarcopenia in Patients with Liver Cirrhosis Meyer, Fatuma Bannert, Karen Wiese, Mats Esau, Susanne Sautter, Lea F. Ehlers, Luise Aghdassi, Ali A. Metges, Cornelia C. Garbe, Leif-A. Jaster, Robert Lerch, Markus M. Lamprecht, Georg Valentini, Luzia Int J Mol Sci Review Liver cirrhosis is frequently accompanied by disease-related malnutrition (DRM) and sarcopenia, defined as loss of skeletal muscle mass and function. DRM and sarcopenia often coexist in cirrhotic patients and are associated with increased morbidity and mortality. The clinical manifestation of both comorbidities are triggered by multifactorial mechanisms including reduced nutrient and energy intake caused by dietary restrictions, anorexia, neuroendocrine deregulation, olfactory and gustatory deficits. Maldigestion and malabsorption due to small intestinal bacterial overgrowth, pancreatic insufficiency or cholestasis may also contribute to DRM and sarcopenia. Decreased protein synthesis and increased protein degradation is the cornerstone mechanism to muscle loss, among others mediated by disease- and inflammation-mediated metabolic changes, hyperammonemia, increased myostatin and reduced human growth hormone. The concise pathophysiological mechanisms and interactions of DRM and sarcopenia in liver cirrhosis are not completely understood. Furthermore, most knowledge in this field are based on experimental models, but only few data in humans exist. This review summarizes known and proposed molecular mechanisms contributing to malnutrition and sarcopenia in liver cirrhosis and highlights remaining knowledge gaps. Since, in the prevention and treatment of DRM and sarcopenia in cirrhotic patients, more research is needed to identify potential biomarkers for diagnosis and development of targeted therapeutic strategies. MDPI 2020-07-28 /pmc/articles/PMC7432938/ /pubmed/32731496 http://dx.doi.org/10.3390/ijms21155357 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Meyer, Fatuma
Bannert, Karen
Wiese, Mats
Esau, Susanne
Sautter, Lea F.
Ehlers, Luise
Aghdassi, Ali A.
Metges, Cornelia C.
Garbe, Leif-A.
Jaster, Robert
Lerch, Markus M.
Lamprecht, Georg
Valentini, Luzia
Molecular Mechanism Contributing to Malnutrition and Sarcopenia in Patients with Liver Cirrhosis
title Molecular Mechanism Contributing to Malnutrition and Sarcopenia in Patients with Liver Cirrhosis
title_full Molecular Mechanism Contributing to Malnutrition and Sarcopenia in Patients with Liver Cirrhosis
title_fullStr Molecular Mechanism Contributing to Malnutrition and Sarcopenia in Patients with Liver Cirrhosis
title_full_unstemmed Molecular Mechanism Contributing to Malnutrition and Sarcopenia in Patients with Liver Cirrhosis
title_short Molecular Mechanism Contributing to Malnutrition and Sarcopenia in Patients with Liver Cirrhosis
title_sort molecular mechanism contributing to malnutrition and sarcopenia in patients with liver cirrhosis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7432938/
https://www.ncbi.nlm.nih.gov/pubmed/32731496
http://dx.doi.org/10.3390/ijms21155357
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