Cachexia induced by cancer and chemotherapy yield distinct perturbations to energy metabolism
Background Cancer cachexia is a metabolic disorder involving perturbed energy balance and altered mitochondrial function. Chemotherapy is a primary treatment option for many types of cancer, but there is substantial evidence that some chemotherapeutic agents can also lead to the development and prog...
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| Vydáno v: | Journal of cachexia, sarcopenia and muscle Ročník 10; číslo 1; s. 140 - 154 |
|---|---|
| Hlavní autoři: | , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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Germany
John Wiley & Sons, Inc
01.02.2019
John Wiley and Sons Inc Wiley |
| Témata: | |
| ISSN: | 2190-5991, 2190-6009, 2190-6009 |
| On-line přístup: | Získat plný text |
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| Abstract | Background
Cancer cachexia is a metabolic disorder involving perturbed energy balance and altered mitochondrial function. Chemotherapy is a primary treatment option for many types of cancer, but there is substantial evidence that some chemotherapeutic agents can also lead to the development and progression of cachexia. In this study, we apply a comprehensive and systems level metabolomics approach to characterize the metabolic perturbations in murine models of cancer‐induced and chemotherapy‐induced cachexia. Knowledge of the unique pathways through which cancer and chemotherapy drive cachexia is necessary in order to develop effective treatments.
Methods
The murine Colon26 (C26) adenocarcinoma xenograft model was used to study the metabolic derangements associated with cancer‐induced cachexia. In vivo administration of Folfiri (5‐fluorouracil, irinotecan, and leucovorin) was used to model chemotherapy‐induced cachexia. Comprehensive metabolic profiling was carried out using both nuclear magnetic resonance‐based and mass spectrometry‐based platforms. Analyses included plasma, muscle, and liver tissue to provide a systems level profiling.
Results
The study involved four groups of CD2F1 male mice (n = 4–5), including vehicle treated (V), C26 tumour hosts (CC), Folfiri treated (F), and C26 tumour hosts treated with Folfiri (CCF). Significant weight loss including skeletal muscle was observed for each of the experimental groups with the tumour hosts showing the most dramatic change (−3.74 g vs. initial body weight in the CC group). Skeletal muscle loss was evident in all experimental groups compared with V, with the CCF combination resulting in the most severe depletion of quadriceps mass (−38% vs. V; P < 0.001). All experimental groups were characterized by an increased systemic glucose demand as evidenced by decreased levels of circulating glucose (−47% in CC vs. V; P < 0.001) and depletion of liver glucose (−51% in CC vs. V; P < 0.001) and glycogen (−74% in CC vs. V; P < 0.001). The cancer‐induced and chemotherapy‐induced cachexia models displayed unique alterations in flux through the tricarboxylic acid cycle and β‐oxidation pathways. Cancer‐induced cachexia was uniquely characterized by a dramatic elevation in low‐density lipoprotein particles (+6.9‐fold vs. V; P < 0.001) and a significant increase in the inflammatory marker, GlycA (+33% vs. V; P < 0.001).
Conclusions
The results of this study demonstrated for the first time that cancer‐induced and chemotherapy‐induced cachexia is characterized by a number of distinct metabolic derangements. Effective therapeutic interventions for cancer‐induced and chemotherapy‐induced cachexia must take into account the specific metabolic defects imposed by the pathological or pharmacological drivers of cachexia. |
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| AbstractList | Cancer cachexia is a metabolic disorder involving perturbed energy balance and altered mitochondrial function. Chemotherapy is a primary treatment option for many types of cancer, but there is substantial evidence that some chemotherapeutic agents can also lead to the development and progression of cachexia. In this study, we apply a comprehensive and systems level metabolomics approach to characterize the metabolic perturbations in murine models of cancer-induced and chemotherapy-induced cachexia. Knowledge of the unique pathways through which cancer and chemotherapy drive cachexia is necessary in order to develop effective treatments.
The murine Colon26 (C26) adenocarcinoma xenograft model was used to study the metabolic derangements associated with cancer-induced cachexia. In vivo administration of Folfiri (5-fluorouracil, irinotecan, and leucovorin) was used to model chemotherapy-induced cachexia. Comprehensive metabolic profiling was carried out using both nuclear magnetic resonance-based and mass spectrometry-based platforms. Analyses included plasma, muscle, and liver tissue to provide a systems level profiling.
The study involved four groups of CD2F1 male mice (n = 4-5), including vehicle treated (V), C26 tumour hosts (CC), Folfiri treated (F), and C26 tumour hosts treated with Folfiri (CCF). Significant weight loss including skeletal muscle was observed for each of the experimental groups with the tumour hosts showing the most dramatic change (-3.74 g vs. initial body weight in the CC group). Skeletal muscle loss was evident in all experimental groups compared with V, with the CCF combination resulting in the most severe depletion of quadriceps mass (-38% vs. V; P < 0.001). All experimental groups were characterized by an increased systemic glucose demand as evidenced by decreased levels of circulating glucose (-47% in CC vs. V; P < 0.001) and depletion of liver glucose (-51% in CC vs. V; P < 0.001) and glycogen (-74% in CC vs. V; P < 0.001). The cancer-induced and chemotherapy-induced cachexia models displayed unique alterations in flux through the tricarboxylic acid cycle and β-oxidation pathways. Cancer-induced cachexia was uniquely characterized by a dramatic elevation in low-density lipoprotein particles (+6.9-fold vs. V; P < 0.001) and a significant increase in the inflammatory marker, GlycA (+33% vs. V; P < 0.001).
The results of this study demonstrated for the first time that cancer-induced and chemotherapy-induced cachexia is characterized by a number of distinct metabolic derangements. Effective therapeutic interventions for cancer-induced and chemotherapy-induced cachexia must take into account the specific metabolic defects imposed by the pathological or pharmacological drivers of cachexia. Abstract Background Cancer cachexia is a metabolic disorder involving perturbed energy balance and altered mitochondrial function. Chemotherapy is a primary treatment option for many types of cancer, but there is substantial evidence that some chemotherapeutic agents can also lead to the development and progression of cachexia. In this study, we apply a comprehensive and systems level metabolomics approach to characterize the metabolic perturbations in murine models of cancer‐induced and chemotherapy‐induced cachexia. Knowledge of the unique pathways through which cancer and chemotherapy drive cachexia is necessary in order to develop effective treatments. Methods The murine Colon26 (C26) adenocarcinoma xenograft model was used to study the metabolic derangements associated with cancer‐induced cachexia. In vivo administration of Folfiri (5‐fluorouracil, irinotecan, and leucovorin) was used to model chemotherapy‐induced cachexia. Comprehensive metabolic profiling was carried out using both nuclear magnetic resonance‐based and mass spectrometry‐based platforms. Analyses included plasma, muscle, and liver tissue to provide a systems level profiling. Results The study involved four groups of CD2F1 male mice (n = 4–5), including vehicle treated (V), C26 tumour hosts (CC), Folfiri treated (F), and C26 tumour hosts treated with Folfiri (CCF). Significant weight loss including skeletal muscle was observed for each of the experimental groups with the tumour hosts showing the most dramatic change (−3.74 g vs. initial body weight in the CC group). Skeletal muscle loss was evident in all experimental groups compared with V, with the CCF combination resulting in the most severe depletion of quadriceps mass (−38% vs. V; P < 0.001). All experimental groups were characterized by an increased systemic glucose demand as evidenced by decreased levels of circulating glucose (−47% in CC vs. V; P < 0.001) and depletion of liver glucose (−51% in CC vs. V; P < 0.001) and glycogen (−74% in CC vs. V; P < 0.001). The cancer‐induced and chemotherapy‐induced cachexia models displayed unique alterations in flux through the tricarboxylic acid cycle and β‐oxidation pathways. Cancer‐induced cachexia was uniquely characterized by a dramatic elevation in low‐density lipoprotein particles (+6.9‐fold vs. V; P < 0.001) and a significant increase in the inflammatory marker, GlycA (+33% vs. V; P < 0.001). Conclusions The results of this study demonstrated for the first time that cancer‐induced and chemotherapy‐induced cachexia is characterized by a number of distinct metabolic derangements. Effective therapeutic interventions for cancer‐induced and chemotherapy‐induced cachexia must take into account the specific metabolic defects imposed by the pathological or pharmacological drivers of cachexia. BackgroundCancer cachexia is a metabolic disorder involving perturbed energy balance and altered mitochondrial function. Chemotherapy is a primary treatment option for many types of cancer, but there is substantial evidence that some chemotherapeutic agents can also lead to the development and progression of cachexia. In this study, we apply a comprehensive and systems level metabolomics approach to characterize the metabolic perturbations in murine models of cancer‐induced and chemotherapy‐induced cachexia. Knowledge of the unique pathways through which cancer and chemotherapy drive cachexia is necessary in order to develop effective treatments.MethodsThe murine Colon26 (C26) adenocarcinoma xenograft model was used to study the metabolic derangements associated with cancer‐induced cachexia. In vivo administration of Folfiri (5‐fluorouracil, irinotecan, and leucovorin) was used to model chemotherapy‐induced cachexia. Comprehensive metabolic profiling was carried out using both nuclear magnetic resonance‐based and mass spectrometry‐based platforms. Analyses included plasma, muscle, and liver tissue to provide a systems level profiling.ResultsThe study involved four groups of CD2F1 male mice (n = 4–5), including vehicle treated (V), C26 tumour hosts (CC), Folfiri treated (F), and C26 tumour hosts treated with Folfiri (CCF). Significant weight loss including skeletal muscle was observed for each of the experimental groups with the tumour hosts showing the most dramatic change (−3.74 g vs. initial body weight in the CC group). Skeletal muscle loss was evident in all experimental groups compared with V, with the CCF combination resulting in the most severe depletion of quadriceps mass (−38% vs. V; P < 0.001). All experimental groups were characterized by an increased systemic glucose demand as evidenced by decreased levels of circulating glucose (−47% in CC vs. V; P < 0.001) and depletion of liver glucose (−51% in CC vs. V; P < 0.001) and glycogen (−74% in CC vs. V; P < 0.001). The cancer‐induced and chemotherapy‐induced cachexia models displayed unique alterations in flux through the tricarboxylic acid cycle and β‐oxidation pathways. Cancer‐induced cachexia was uniquely characterized by a dramatic elevation in low‐density lipoprotein particles (+6.9‐fold vs. V; P < 0.001) and a significant increase in the inflammatory marker, GlycA (+33% vs. V; P < 0.001).ConclusionsThe results of this study demonstrated for the first time that cancer‐induced and chemotherapy‐induced cachexia is characterized by a number of distinct metabolic derangements. Effective therapeutic interventions for cancer‐induced and chemotherapy‐induced cachexia must take into account the specific metabolic defects imposed by the pathological or pharmacological drivers of cachexia. Cancer cachexia is a metabolic disorder involving perturbed energy balance and altered mitochondrial function. Chemotherapy is a primary treatment option for many types of cancer, but there is substantial evidence that some chemotherapeutic agents can also lead to the development and progression of cachexia. In this study, we apply a comprehensive and systems level metabolomics approach to characterize the metabolic perturbations in murine models of cancer-induced and chemotherapy-induced cachexia. Knowledge of the unique pathways through which cancer and chemotherapy drive cachexia is necessary in order to develop effective treatments.BACKGROUNDCancer cachexia is a metabolic disorder involving perturbed energy balance and altered mitochondrial function. Chemotherapy is a primary treatment option for many types of cancer, but there is substantial evidence that some chemotherapeutic agents can also lead to the development and progression of cachexia. In this study, we apply a comprehensive and systems level metabolomics approach to characterize the metabolic perturbations in murine models of cancer-induced and chemotherapy-induced cachexia. Knowledge of the unique pathways through which cancer and chemotherapy drive cachexia is necessary in order to develop effective treatments.The murine Colon26 (C26) adenocarcinoma xenograft model was used to study the metabolic derangements associated with cancer-induced cachexia. In vivo administration of Folfiri (5-fluorouracil, irinotecan, and leucovorin) was used to model chemotherapy-induced cachexia. Comprehensive metabolic profiling was carried out using both nuclear magnetic resonance-based and mass spectrometry-based platforms. Analyses included plasma, muscle, and liver tissue to provide a systems level profiling.METHODSThe murine Colon26 (C26) adenocarcinoma xenograft model was used to study the metabolic derangements associated with cancer-induced cachexia. In vivo administration of Folfiri (5-fluorouracil, irinotecan, and leucovorin) was used to model chemotherapy-induced cachexia. Comprehensive metabolic profiling was carried out using both nuclear magnetic resonance-based and mass spectrometry-based platforms. Analyses included plasma, muscle, and liver tissue to provide a systems level profiling.The study involved four groups of CD2F1 male mice (n = 4-5), including vehicle treated (V), C26 tumour hosts (CC), Folfiri treated (F), and C26 tumour hosts treated with Folfiri (CCF). Significant weight loss including skeletal muscle was observed for each of the experimental groups with the tumour hosts showing the most dramatic change (-3.74 g vs. initial body weight in the CC group). Skeletal muscle loss was evident in all experimental groups compared with V, with the CCF combination resulting in the most severe depletion of quadriceps mass (-38% vs. V; P < 0.001). All experimental groups were characterized by an increased systemic glucose demand as evidenced by decreased levels of circulating glucose (-47% in CC vs. V; P < 0.001) and depletion of liver glucose (-51% in CC vs. V; P < 0.001) and glycogen (-74% in CC vs. V; P < 0.001). The cancer-induced and chemotherapy-induced cachexia models displayed unique alterations in flux through the tricarboxylic acid cycle and β-oxidation pathways. Cancer-induced cachexia was uniquely characterized by a dramatic elevation in low-density lipoprotein particles (+6.9-fold vs. V; P < 0.001) and a significant increase in the inflammatory marker, GlycA (+33% vs. V; P < 0.001).RESULTSThe study involved four groups of CD2F1 male mice (n = 4-5), including vehicle treated (V), C26 tumour hosts (CC), Folfiri treated (F), and C26 tumour hosts treated with Folfiri (CCF). Significant weight loss including skeletal muscle was observed for each of the experimental groups with the tumour hosts showing the most dramatic change (-3.74 g vs. initial body weight in the CC group). Skeletal muscle loss was evident in all experimental groups compared with V, with the CCF combination resulting in the most severe depletion of quadriceps mass (-38% vs. V; P < 0.001). All experimental groups were characterized by an increased systemic glucose demand as evidenced by decreased levels of circulating glucose (-47% in CC vs. V; P < 0.001) and depletion of liver glucose (-51% in CC vs. V; P < 0.001) and glycogen (-74% in CC vs. V; P < 0.001). The cancer-induced and chemotherapy-induced cachexia models displayed unique alterations in flux through the tricarboxylic acid cycle and β-oxidation pathways. Cancer-induced cachexia was uniquely characterized by a dramatic elevation in low-density lipoprotein particles (+6.9-fold vs. V; P < 0.001) and a significant increase in the inflammatory marker, GlycA (+33% vs. V; P < 0.001).The results of this study demonstrated for the first time that cancer-induced and chemotherapy-induced cachexia is characterized by a number of distinct metabolic derangements. Effective therapeutic interventions for cancer-induced and chemotherapy-induced cachexia must take into account the specific metabolic defects imposed by the pathological or pharmacological drivers of cachexia.CONCLUSIONSThe results of this study demonstrated for the first time that cancer-induced and chemotherapy-induced cachexia is characterized by a number of distinct metabolic derangements. Effective therapeutic interventions for cancer-induced and chemotherapy-induced cachexia must take into account the specific metabolic defects imposed by the pathological or pharmacological drivers of cachexia. Background Cancer cachexia is a metabolic disorder involving perturbed energy balance and altered mitochondrial function. Chemotherapy is a primary treatment option for many types of cancer, but there is substantial evidence that some chemotherapeutic agents can also lead to the development and progression of cachexia. In this study, we apply a comprehensive and systems level metabolomics approach to characterize the metabolic perturbations in murine models of cancer‐induced and chemotherapy‐induced cachexia. Knowledge of the unique pathways through which cancer and chemotherapy drive cachexia is necessary in order to develop effective treatments. Methods The murine Colon26 (C26) adenocarcinoma xenograft model was used to study the metabolic derangements associated with cancer‐induced cachexia. In vivo administration of Folfiri (5‐fluorouracil, irinotecan, and leucovorin) was used to model chemotherapy‐induced cachexia. Comprehensive metabolic profiling was carried out using both nuclear magnetic resonance‐based and mass spectrometry‐based platforms. Analyses included plasma, muscle, and liver tissue to provide a systems level profiling. Results The study involved four groups of CD2F1 male mice (n = 4–5), including vehicle treated (V), C26 tumour hosts (CC), Folfiri treated (F), and C26 tumour hosts treated with Folfiri (CCF). Significant weight loss including skeletal muscle was observed for each of the experimental groups with the tumour hosts showing the most dramatic change (−3.74 g vs. initial body weight in the CC group). Skeletal muscle loss was evident in all experimental groups compared with V, with the CCF combination resulting in the most severe depletion of quadriceps mass (−38% vs. V; P < 0.001). All experimental groups were characterized by an increased systemic glucose demand as evidenced by decreased levels of circulating glucose (−47% in CC vs. V; P < 0.001) and depletion of liver glucose (−51% in CC vs. V; P < 0.001) and glycogen (−74% in CC vs. V; P < 0.001). The cancer‐induced and chemotherapy‐induced cachexia models displayed unique alterations in flux through the tricarboxylic acid cycle and β‐oxidation pathways. Cancer‐induced cachexia was uniquely characterized by a dramatic elevation in low‐density lipoprotein particles (+6.9‐fold vs. V; P < 0.001) and a significant increase in the inflammatory marker, GlycA (+33% vs. V; P < 0.001). Conclusions The results of this study demonstrated for the first time that cancer‐induced and chemotherapy‐induced cachexia is characterized by a number of distinct metabolic derangements. Effective therapeutic interventions for cancer‐induced and chemotherapy‐induced cachexia must take into account the specific metabolic defects imposed by the pathological or pharmacological drivers of cachexia. |
| Author | Bonetto, Andrea Pin, Fabrizio Barreto, Rafael O'Connell, Thomas M. Couch, Marion E. |
| AuthorAffiliation | 3 Department of Surgery Indiana University School of Medicine Indianapolis USA 5 Simon Cancer Center Indiana University School of Medicine Indianapolis USA 2 Indiana Center for Musculoskeletal Health Indiana University School of Medicine Indianapolis USA 1 Department of Anatomy and Cell Biology Indiana University School of Medicine Indianapolis USA 4 Department of Otolaryngology–Head & Neck Surgery Indiana University School of Medicine Indianapolis USA 6 IUPUI Center for Cachexia Research, Innovation and Therapy Indiana University School of Medicine Indianapolis USA |
| AuthorAffiliation_xml | – name: 1 Department of Anatomy and Cell Biology Indiana University School of Medicine Indianapolis USA – name: 5 Simon Cancer Center Indiana University School of Medicine Indianapolis USA – name: 6 IUPUI Center for Cachexia Research, Innovation and Therapy Indiana University School of Medicine Indianapolis USA – name: 2 Indiana Center for Musculoskeletal Health Indiana University School of Medicine Indianapolis USA – name: 3 Department of Surgery Indiana University School of Medicine Indianapolis USA – name: 4 Department of Otolaryngology–Head & Neck Surgery Indiana University School of Medicine Indianapolis USA |
| Author_xml | – sequence: 1 givenname: Fabrizio surname: Pin fullname: Pin, Fabrizio organization: Indiana University School of Medicine – sequence: 2 givenname: Rafael surname: Barreto fullname: Barreto, Rafael organization: Indiana University School of Medicine – sequence: 3 givenname: Marion E. surname: Couch fullname: Couch, Marion E. organization: Indiana University School of Medicine – sequence: 4 givenname: Andrea orcidid: 0000-0002-3235-1871 surname: Bonetto fullname: Bonetto, Andrea email: abonetto@iu.edu organization: Indiana University School of Medicine – sequence: 5 givenname: Thomas M. orcidid: 0000-0003-4342-9539 surname: O'Connell fullname: O'Connell, Thomas M. email: thoconnell@iu.edu organization: Indiana University School of Medicine |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30680954$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1007/s11306-012-0485-6 10.1016/S0014-5793(98)01178-8 10.1016/j.febslet.2005.02.017 10.1177/1099800414558087 10.1038/sj.embor.7400532 10.1371/journal.pone.0165615 10.1152/physiol.00046.2010 10.1152/japplphysiol.01138.2006 10.1097/MCO.0000000000000164 10.1002/jcsm.12261 10.1152/physrev.00031.2007 10.1152/japplphysiol.01318.2003 10.1093/jnci/92.4.321 10.3389/fphys.2016.00472 10.1089/ars.2011.3965 10.1186/s13075-016-0982-5 10.1038/nprot.2007.376 10.1007/BF00917463 10.1038/nrc927 10.3892/ijo.2013.1998 10.1016/0300-9084(91)90081-B 10.1002/ijc.23754 10.1021/pr1002774 10.1016/j.bbrc.2003.07.013 10.1038/sj.bjc.6600074 10.1046/j.1523-1755.2003.00281.x 10.1016/S1470-2045(10)70218-7 10.1172/JCI118657 10.1016/S0261-5614(96)80028-8 10.1038/bonekey.2015.101 10.1007/s13539-012-0101-7 10.3389/fphys.2014.00503 10.1152/ajpendo.00039.2012 10.1038/ki.1997.263 10.1002/jcsm.12023 10.1038/nm.4093 10.1016/j.cmet.2006.02.002 10.1200/JCO.20.2.371 10.1016/0014-5793(87)80168-0 10.2337/db11-1355 10.1371/journal.pone.0022538 10.1016/j.cmet.2007.10.013 10.1097/MCO.0000000000000106 10.1172/JCI114421 10.1038/sj.bjc.6600101 10.1210/en.2013-1179 10.18632/oncotarget.6439 10.1016/j.cll.2006.07.006 10.1007/s11306-008-0113-7 10.1016/0026-0495(95)90040-3 10.1373/clinchem.2014.232918 10.1242/dmm.008839 10.1016/S0168-8278(97)80124-9 10.1016/j.clnu.2008.06.013 10.18632/oncotarget.9779 |
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| Copyright | 2019 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by John Wiley & Sons Ltd on behalf of the Society on Sarcopenia, Cachexia and Wasting Disorders 2019 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by John Wiley & Sons Ltd on behalf of the Society on Sarcopenia, Cachexia and Wasting Disorders. 2019. This work is published under http://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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| References | 2012; 61 2001; 50 2007; 102 2017; 8 2012; 2012 2013; 4 2005; 579 2008; 7 2000; 92 2011; 12 2011; 15 1998; 436 2008; 4 1989; 49 2013; 9 1990; 85 2014; 5 1997; 51 2002; 86 2008; 27 2006; 26 2016; 117 2013; 154 2007; 2 2011; 26 2014; 17 2011; 27 2010; 9 2015; 6 2015; 17 2015; 4 2015; 18 2013; 43 2008; 18 1997; 26 1991; 73 2002; 2 2006; 3 2008; 123 2016; 18 2011; 6 2012; 303 1996; 15 1996; 97 2016; 11 2004; 96 2016; 7 2004; 313 1987; 215 2002; 20 2015; 61 1995; 44 2005; 6 2008; 88 1994; 1 2012; 5 2003; 64 2016; 22 2005; 14 e_1_2_9_31_1 e_1_2_9_52_1 e_1_2_9_50_1 e_1_2_9_10_1 e_1_2_9_35_1 e_1_2_9_56_1 e_1_2_9_12_1 e_1_2_9_33_1 Constantinou C (e_1_2_9_37_1) 2011; 27 e_1_2_9_54_1 Damrauer JS (e_1_2_9_11_1) 2008; 18 e_1_2_9_14_1 e_1_2_9_39_1 e_1_2_9_16_1 e_1_2_9_58_1 e_1_2_9_18_1 Holecek M (e_1_2_9_32_1) 2001; 50 e_1_2_9_41_1 DeJong CH (e_1_2_9_62_1) 2005; 14 e_1_2_9_20_1 e_1_2_9_22_1 e_1_2_9_45_1 e_1_2_9_24_1 e_1_2_9_43_1 e_1_2_9_8_1 e_1_2_9_6_1 e_1_2_9_4_1 e_1_2_9_60_1 e_1_2_9_2_1 ultani M (e_1_2_9_15_1) 2012; 2012 Beck SA (e_1_2_9_30_1) 1989; 49 e_1_2_9_26_1 e_1_2_9_49_1 e_1_2_9_28_1 e_1_2_9_47_1 e_1_2_9_53_1 e_1_2_9_51_1 e_1_2_9_34_1 e_1_2_9_57_1 e_1_2_9_13_1 e_1_2_9_55_1 e_1_2_9_38_1 e_1_2_9_17_1 e_1_2_9_36_1 e_1_2_9_59_1 e_1_2_9_42_1 e_1_2_9_63_1 e_1_2_9_40_1 e_1_2_9_61_1 Bonetto A (e_1_2_9_19_1) 2016; 117 e_1_2_9_21_1 e_1_2_9_46_1 e_1_2_9_23_1 e_1_2_9_44_1 e_1_2_9_7_1 e_1_2_9_5_1 e_1_2_9_3_1 e_1_2_9_9_1 e_1_2_9_25_1 e_1_2_9_27_1 e_1_2_9_48_1 e_1_2_9_29_1 |
| References_xml | – volume: 73 start-page: 99 year: 1991 end-page: 104 article-title: Variations of plasma sialic acid and ‐acetylglucosamine levels in cancer, inflammatory diseases and bone marrow transplantation: a proton NMR spectroscopy study publication-title: Biochimie – volume: 4 start-page: 216 year: 2008 end-page: 225 article-title: Metabolomic analysis of cancer cachexia reveals distinct lipid and glucose alterations publication-title: Metabolomics – volume: 14 start-page: 257 year: 2005 end-page: 263 article-title: Systemic inflammation correlates with increased expression of skeletal muscle ubiquitin but not uncoupling proteins in cancer cachexia publication-title: Oncol Rep – volume: 49 start-page: 3800 year: 1989 end-page: 3804 article-title: Nitrogen excretion in cancer cachexia and its modification by a high fat diet in mice publication-title: Cancer Res – volume: 15 start-page: 91 year: 1996 end-page: 93 article-title: Leucine metabolism in fasted and tumor necrosis factor‐treated rats publication-title: Clin Nutr – volume: 64 start-page: 1780 year: 2003 end-page: 1786 article-title: Protein restriction and AST‐120 improve lipoprotein lipase and VLDL receptor in focal glomerulosclerosis publication-title: Kidney Int – volume: 7 start-page: 472 year: 2016 article-title: Cancer and chemotherapy contribute to muscle loss by activating common signaling pathways publication-title: Front Physiol. – volume: 51 start-page: 1933 year: 1997 end-page: 1937 article-title: Down‐regulation of hepatic lipase expression in experimental nephrotic syndrome publication-title: Kidney Int – volume: 303 start-page: E410 year: 2012 end-page: E421 article-title: JAK/STAT3 pathway inhibition blocks skeletal muscle wasting downstream of IL‐6 and in experimental cancer cachexia publication-title: Am J Physiol Endocrinol Metab – volume: 18 start-page: 139 year: 2008 end-page: 148 article-title: Chemotherapy‐induced muscle wasting: association with NF‐κB and cancer cachexia publication-title: Basic Applied Myology – volume: 7 start-page: 45 year: 2008 end-page: 56 article-title: Mitochondrial overload and incomplete fatty acid oxidation contribute to skeletal muscle insulin resistance publication-title: Cell Metab – volume: 11 year: 2016 article-title: Association of N‐linked glycoprotein acetyls and colorectal cancer incidence and mortality publication-title: PloS one – volume: 50 start-page: 25 year: 2001 end-page: 33 article-title: Metabolism of branched‐chain amino acids in starved rats: the role of hepatic tissue publication-title: Physiol Res – volume: 6 start-page: 132 year: 2015 end-page: 143 article-title: Ghrelin prevents tumour‐ and cisplatin‐induced muscle wasting: characterization of multiple mechanisms involved publication-title: J Cachexia Sarcopenia Muscle – volume: 44 start-page: 1340 year: 1995 end-page: 1348 article-title: Negative impact of cancer chemotherapy on protein metabolism in healthy and tumor‐bearing rats publication-title: Metabolism: clinical and experimental – volume: 22 start-page: 666 year: 2016 end-page: 671 article-title: Excessive fatty acid oxidation induces muscle atrophy in cancer cachexia publication-title: Nat Med – volume: 96 start-page: 2082 issue: 6 year: 2004 end-page: 2087 article-title: Pyruvate dehydrogenase activation and kinase expression in human skeletal muscle during fasting publication-title: J Appl Physiol – volume: 5 start-page: 503 year: 2014 article-title: Mitochondria dysfunction in lung cancer‐induced muscle wasting in C2C12 myotubes publication-title: Front Physiol – volume: 9 start-page: 4545 year: 2010 end-page: 4553 article-title: 1H NMR spectroscopy‐based interventional metabolic phenotyping: a cohort study of rheumatoid arthritis patients publication-title: J Proteome Res – volume: 27 start-page: 15 year: 2011 end-page: 24 article-title: Nuclear magnetic resonance in conjunction with functional genomics suggests mitochondrial dysfunction in a murine model of cancer cachexia publication-title: Int J Mol Med – volume: 92 start-page: 321 year: 2000 end-page: 328 article-title: Randomized clinical trial of adenosine 5′‐triphosphate in patients with advanced non‐small‐cell lung cancer publication-title: J Natl Cancer Inst – volume: 27 start-page: 793 year: 2008 end-page: 799 article-title: Cachexia: a new definition publication-title: Clin Nutr – volume: 5 start-page: 533 year: 2012 end-page: 545 article-title: Importance of functional and metabolic impairments in the characterization of the C‐26 murine model of cancer cachexia publication-title: Dis Model Mech – volume: 117 year: 2016 article-title: The Colon‐26 carcinoma tumor‐bearing mouse as a model for the study of cancer cachexia publication-title: Journal of visualized experiments: JoVE – volume: 2 start-page: 2692 issue: 11 year: 2007 end-page: 703 article-title: Metabolic profiling, metabolomic and metabonomic procedures for NMR spectroscopy of urine, plasma, serum and tissue extracts publication-title: Nat Protoc. – volume: 313 start-page: 417 year: 2004 end-page: 422 article-title: Regulation of protein synthesis by branched‐chain amino acids publication-title: Biochem Biophys Res Commun – volume: 436 start-page: 415 year: 1998 end-page: 418 article-title: Skeletal muscle UCP2 and UCP3 gene expression in a rat cancer cachexia model publication-title: FEBS Lett – volume: 17 start-page: 509 year: 2014 end-page: 514 article-title: The energy balance in cancer cachexia revisited publication-title: Curr Opin Clin Nutr Metab Care – volume: 2012 start-page: 490804 year: 2012 article-title: Anti‐inflammatory cytokines: important immunoregulatory factors contributing to chemotherapy‐induced gastrointestinal mucositis publication-title: Chemother Res Pract – volume: 88 start-page: 1243 year: 2008 end-page: 1276 article-title: Exercise‐induced oxidative stress: cellular mechanisms and impact on muscle force production publication-title: Physiol Rev – volume: 4 start-page: 145 year: 2013 end-page: 155 article-title: Metabolic derangements in the gastrocnemius and the effect of compound A therapy in a murine model of cancer cachexia publication-title: J Cachexia Sarcopenia Muscle – volume: 26 start-page: 1141 year: 1997 end-page: 1147 article-title: Leucine metabolism in partially hepatectomized rats publication-title: J Hepatol – volume: 18 start-page: 86 year: 2016 article-title: A novel inflammatory biomarker, GlycA, associates with disease activity in rheumatoid arthritis and cardio‐metabolic risk in BMI‐matched controls publication-title: Arthritis Res Ther – volume: 20 start-page: 371 year: 2002 end-page: 378 article-title: Beneficial effects of adenosine triphosphate on nutritional status in advanced lung cancer patients: a randomized clinical trial publication-title: J Clin Oncol – volume: 18 start-page: 221 year: 2015 end-page: 225 article-title: Muscle wasting in cancer: the role of mitochondria publication-title: Curr Opin Clin Nutr Metab Care – volume: 4 start-page: 732 year: 2015 article-title: Assessment of muscle mass and strength in mice publication-title: Bonekey Rep – volume: 3 start-page: 177 year: 2006 end-page: 185 article-title: HIF‐1‐mediated expression of pyruvate dehydrogenase kinase: a metabolic switch required for cellular adaptation to hypoxia publication-title: Cell Metab – volume: 123 start-page: 1227 year: 2008 end-page: 1239 article-title: Impact of antioxidant supplementation on chemotherapeutic toxicity: a systematic review of the evidence from randomized controlled trials publication-title: Int J Cancer – volume: 7 start-page: 43442 year: 2016 end-page: 43460 article-title: Chemotherapy‐related cachexia is associated with mitochondrial depletion and the activation of ERK1/2 and p38 MAPKs publication-title: Oncotarget. – volume: 17 start-page: 549 year: 2015 end-page: 557 article-title: Induction of IL‐6 by cytotoxic chemotherapy is associated with loss of lean body and fat mass in tumor‐free female mice publication-title: Biol Res Nurs – volume: 86 start-page: 612 year: 2002 end-page: 618 article-title: Expression of uncoupling proteins‐1, ‐2 and ‐3 mRNA is induced by an adenocarcinoma‐derived lipid‐mobilizing factor publication-title: Br J Cancer – volume: 86 start-page: 372 year: 2002 end-page: 375 article-title: Muscle UCP‐3 mRNA levels are elevated in weight loss associated with gastrointestinal adenocarcinoma in humans publication-title: Br J Cancer – volume: 102 start-page: 2056 year: 2007 end-page: 2063 article-title: Free radical‐mediated skeletal muscle dysfunction in inflammatory conditions publication-title: J Appl Physiol – volume: 61 start-page: 714 year: 2015 end-page: 723 article-title: GlycA: a composite nuclear magnetic resonance biomarker of systemic inflammation publication-title: Clin Chem – volume: 8 start-page: 1081 year: 2017 end-page: 1083 article-title: Ethical guidelines for publishing in the Journal of Cachexia, Sarcopenia and Muscle: update 2017 publication-title: J Cachexia Sarcopenia Muscle – volume: 6 start-page: e22538 year: 2011 article-title: STAT3 activation in skeletal muscle links muscle wasting and the acute phase response in cancer cachexia publication-title: PloS one. – volume: 12 start-page: 489 year: 2011 end-page: 495 article-title: Definition and classification of cancer cachexia: an international consensus publication-title: Lancet Oncol – volume: 9 start-page: 730 year: 2013 end-page: 739 article-title: Cancer cachexia's metabolic signature in a murine model confirms a distinct entity publication-title: Metabolomics. – volume: 6 start-page: 917 year: 2005 end-page: 921 article-title: Uncoupling proteins: current status and therapeutic prospects publication-title: EMBO Rep – volume: 26 start-page: 847 year: 2006 end-page: 870 article-title: Lipoprotein particle analysis by nuclear magnetic resonance spectroscopy publication-title: Clin Lab Med – volume: 43 start-page: 886 year: 2013 end-page: 894 article-title: Skeletal muscle mitochondrial uncoupling in a murine cancer cachexia model publication-title: Int J Oncol – volume: 215 start-page: 311 year: 1987 end-page: 315 article-title: Assignment of resonances for ‘acute‐phase’ glycoproteins in high resolution proton NMR spectra of human blood plasma publication-title: FEBS Lett – volume: 2 start-page: 862 year: 2002 end-page: 871 article-title: Cachexia in cancer patients publication-title: Nat Rev Cancer – volume: 1 start-page: 5 year: 1994 end-page: 14 article-title: Changes in glycosylation of acute‐phase proteins in health and disease: occurence, regulation and function publication-title: Glycoconj J – volume: 26 start-page: 192 year: 2011 end-page: 205 article-title: The regulation and physiology of mitochondrial proton leak publication-title: Physiology (Bethesda) – volume: 61 start-page: 1372 year: 2012 end-page: 1380 article-title: Metabolic signatures of insulin resistance in 7,098 young adults publication-title: Diabetes – volume: 154 start-page: 3118 year: 2013 end-page: 3129 article-title: Inhibition of cisplatin‐induced lipid catabolism and weight loss by ghrelin in male mice publication-title: Endocrinology – volume: 85 start-page: 256 year: 1990 end-page: 263 article-title: Administration of endotoxin, tumor necrosis factor, or interleukin 1 to rats activates skeletal muscle branched‐chain alpha‐keto acid dehydrogenase publication-title: J Clin Invest – volume: 579 start-page: 1646 year: 2005 end-page: 1652 article-title: Both oxidative and nitrosative stress are associated with muscle wasting in tumour‐bearing rats publication-title: FEBS Lett – volume: 97 start-page: 2167 year: 1996 end-page: 2173 article-title: Abnormalities in hepatic lipase in chronic renal failure: role of excess parathyroid hormone publication-title: J Clin Invest – volume: 15 start-page: 2543 year: 2011 end-page: 2563 article-title: Chemotherapy‐induced weakness and fatigue in skeletal muscle: the role of oxidative stress publication-title: Antioxid Redox Signal – volume: 6 start-page: 43202 year: 2015 end-page: 43215 article-title: Combination of exercise training and erythropoietin prevents cancer‐induced muscle alterations publication-title: Oncotarget – ident: e_1_2_9_26_1 doi: 10.1007/s11306-012-0485-6 – ident: e_1_2_9_41_1 doi: 10.1016/S0014-5793(98)01178-8 – ident: e_1_2_9_49_1 doi: 10.1016/j.febslet.2005.02.017 – ident: e_1_2_9_61_1 doi: 10.1177/1099800414558087 – ident: e_1_2_9_43_1 doi: 10.1038/sj.embor.7400532 – ident: e_1_2_9_56_1 doi: 10.1371/journal.pone.0165615 – volume: 14 start-page: 257 year: 2005 ident: e_1_2_9_62_1 article-title: Systemic inflammation correlates with increased expression of skeletal muscle ubiquitin but not uncoupling proteins in cancer cachexia publication-title: Oncol Rep – volume: 27 start-page: 15 year: 2011 ident: e_1_2_9_37_1 article-title: Nuclear magnetic resonance in conjunction with functional genomics suggests mitochondrial dysfunction in a murine model of cancer cachexia publication-title: Int J Mol Med – ident: e_1_2_9_42_1 doi: 10.1152/physiol.00046.2010 – ident: e_1_2_9_52_1 doi: 10.1152/japplphysiol.01138.2006 – ident: e_1_2_9_8_1 doi: 10.1097/MCO.0000000000000164 – ident: e_1_2_9_63_1 doi: 10.1002/jcsm.12261 – ident: e_1_2_9_51_1 doi: 10.1152/physrev.00031.2007 – ident: e_1_2_9_28_1 doi: 10.1152/japplphysiol.01318.2003 – ident: e_1_2_9_44_1 doi: 10.1093/jnci/92.4.321 – ident: e_1_2_9_6_1 doi: 10.3389/fphys.2016.00472 – ident: e_1_2_9_14_1 doi: 10.1089/ars.2011.3965 – ident: e_1_2_9_60_1 doi: 10.1186/s13075-016-0982-5 – volume: 49 start-page: 3800 year: 1989 ident: e_1_2_9_30_1 article-title: Nitrogen excretion in cancer cachexia and its modification by a high fat diet in mice publication-title: Cancer Res – ident: e_1_2_9_22_1 doi: 10.1038/nprot.2007.376 – ident: e_1_2_9_59_1 doi: 10.1007/BF00917463 – ident: e_1_2_9_3_1 doi: 10.1038/nrc927 – ident: e_1_2_9_29_1 doi: 10.3892/ijo.2013.1998 – ident: e_1_2_9_55_1 doi: 10.1016/0300-9084(91)90081-B – volume: 2012 start-page: 490804 year: 2012 ident: e_1_2_9_15_1 article-title: Anti‐inflammatory cytokines: important immunoregulatory factors contributing to chemotherapy‐induced gastrointestinal mucositis publication-title: Chemother Res Pract – ident: e_1_2_9_50_1 doi: 10.1002/ijc.23754 – ident: e_1_2_9_54_1 doi: 10.1021/pr1002774 – ident: e_1_2_9_31_1 doi: 10.1016/j.bbrc.2003.07.013 – ident: e_1_2_9_40_1 doi: 10.1038/sj.bjc.6600074 – ident: e_1_2_9_48_1 doi: 10.1046/j.1523-1755.2003.00281.x – ident: e_1_2_9_2_1 doi: 10.1016/S1470-2045(10)70218-7 – ident: e_1_2_9_46_1 doi: 10.1172/JCI118657 – ident: e_1_2_9_33_1 doi: 10.1016/S0261-5614(96)80028-8 – ident: e_1_2_9_21_1 doi: 10.1038/bonekey.2015.101 – ident: e_1_2_9_17_1 doi: 10.1007/s13539-012-0101-7 – volume: 18 start-page: 139 year: 2008 ident: e_1_2_9_11_1 article-title: Chemotherapy‐induced muscle wasting: association with NF‐κB and cancer cachexia publication-title: Basic Applied Myology – volume: 50 start-page: 25 year: 2001 ident: e_1_2_9_32_1 article-title: Metabolism of branched‐chain amino acids in starved rats: the role of hepatic tissue publication-title: Physiol Res – ident: e_1_2_9_38_1 doi: 10.3389/fphys.2014.00503 – ident: e_1_2_9_58_1 doi: 10.1152/ajpendo.00039.2012 – ident: e_1_2_9_47_1 doi: 10.1038/ki.1997.263 – ident: e_1_2_9_12_1 doi: 10.1002/jcsm.12023 – ident: e_1_2_9_18_1 doi: 10.1038/nm.4093 – ident: e_1_2_9_27_1 doi: 10.1016/j.cmet.2006.02.002 – ident: e_1_2_9_45_1 doi: 10.1200/JCO.20.2.371 – ident: e_1_2_9_53_1 doi: 10.1016/0014-5793(87)80168-0 – ident: e_1_2_9_57_1 doi: 10.2337/db11-1355 – ident: e_1_2_9_20_1 doi: 10.1371/journal.pone.0022538 – ident: e_1_2_9_36_1 doi: 10.1016/j.cmet.2007.10.013 – ident: e_1_2_9_9_1 doi: 10.1097/MCO.0000000000000106 – ident: e_1_2_9_35_1 doi: 10.1172/JCI114421 – volume: 117 year: 2016 ident: e_1_2_9_19_1 article-title: The Colon‐26 carcinoma tumor‐bearing mouse as a model for the study of cancer cachexia publication-title: Journal of visualized experiments: JoVE – ident: e_1_2_9_39_1 doi: 10.1038/sj.bjc.6600101 – ident: e_1_2_9_13_1 doi: 10.1210/en.2013-1179 – ident: e_1_2_9_5_1 doi: 10.18632/oncotarget.6439 – ident: e_1_2_9_23_1 doi: 10.1016/j.cll.2006.07.006 – ident: e_1_2_9_16_1 doi: 10.1007/s11306-008-0113-7 – ident: e_1_2_9_10_1 doi: 10.1016/0026-0495(95)90040-3 – ident: e_1_2_9_24_1 doi: 10.1373/clinchem.2014.232918 – ident: e_1_2_9_25_1 doi: 10.1242/dmm.008839 – ident: e_1_2_9_34_1 doi: 10.1016/S0168-8278(97)80124-9 – ident: e_1_2_9_4_1 doi: 10.1016/j.clnu.2008.06.013 – ident: e_1_2_9_7_1 doi: 10.18632/oncotarget.9779 |
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Cancer cachexia is a metabolic disorder involving perturbed energy balance and altered mitochondrial function. Chemotherapy is a primary treatment... Cancer cachexia is a metabolic disorder involving perturbed energy balance and altered mitochondrial function. Chemotherapy is a primary treatment option for... BackgroundCancer cachexia is a metabolic disorder involving perturbed energy balance and altered mitochondrial function. Chemotherapy is a primary treatment... Abstract Background Cancer cachexia is a metabolic disorder involving perturbed energy balance and altered mitochondrial function. Chemotherapy is a primary... |
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| SubjectTerms | Animals Anorexia Antineoplastic Agents - adverse effects Antineoplastic Combined Chemotherapy Protocols - adverse effects Cachexia Cachexia - chemically induced Cachexia - metabolism Cachexia - pathology Camptothecin - adverse effects Camptothecin - analogs & derivatives Cancer Cancer therapies Cell Line, Tumor Chemotherapy Dehydrogenases Energy Metabolism Fluorouracil - adverse effects Glucose - metabolism Laboratory animals Leucovorin - adverse effects Lipids Liver Liver - drug effects Liver - metabolism Male Metabolism Metabolites Metabolomics Mice Muscle Strength Muscle wasting Muscle, Skeletal - drug effects Muscle, Skeletal - metabolism Muscle, Skeletal - pathology Musculoskeletal system Neoplasms - chemically induced Neoplasms - metabolism Neoplasms - pathology Nitrogen NMR Nuclear magnetic resonance Original Oxidative stress Reactive Oxygen Species - metabolism Receptors, LDL - metabolism Studies |
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| Title | Cachexia induced by cancer and chemotherapy yield distinct perturbations to energy metabolism |
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