Liver lipid metabolism disruption in cancer cachexia is aggravated by cla supplementation -induced inflammation
Autor(a) principal: | |
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Data de Publicação: | 2019 |
Outros Autores: | , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNESP |
Texto Completo: | http://dx.doi.org/10.1016/j.clnu.2018.09.023 http://hdl.handle.net/11449/196274 |
Resumo: | Background & aims: The liver is the main organ regulating metabolism. In spite of that, few studies examine liver metabolism in cachexia, a wasting syndrome associated with increased morbidity and mortality in cancer. Cachexia induces major metabolic disruption, inflammation and fat and lean mass loss. We have previously shown impairment of hepatic lipid metabolism in cancer cachexia that contributes to the aggravation of the symptoms. The present study addresses the effects of Conjugated Linoleic Acid supplementation upon liver lipid metabolism in cachectic rats. Methods: Male Wistar rats were randomly assigned to control groups (C) receiving 0.9 NaCl (Placebo -CP); or to groups supplemented with sunflower oil (CSF), supplemented with CLA (CCLA), or still, to tumour bearing animals (T) receiving NaCl (TP), sunflower oil (TSF), or CLA (TCLA). Supplementation (0.5 ml) by gavage was carried out for 14 days. Body weight, dietary intake, glucose, cholesterol and triacylglycerol plasma content, liver glycogen and triacylglycerol content and mRNA expression of liver carnitine palmitoyltransferase I and II (CPT I and II), as well as microsomal triglyceride transfer protein (MTP), liver fatty acid-binding protein (L-FABP), peroxisome proliferator-activated receptor-alpha (PPAR-alpha), and apolipoprotein B (apoB), were assessed. Results: Liver CPT II activity was reduced in all groups, when compared with CP. Hepatic mRNA expression of MTP, apoB and FABP was reduced in TCLA, when compared with all groups. TCLA also presented increased hepatic and plasma triacylglycerol content, when compared with all T groups. Adipose tissue-derived inflammatory factors were assessed. No differences among the groups were observed in regard to Retro Peritoneal Adipose Tissue cytokine (IL-1 beta, IL-6, and TNF-alpha) protein content and expression, with the exception of IL-10 in tumour-bearing animals. In the Epididymal Adipose Tissue, the inflammatory cytokines were augmented in TCLA, compared with all other groups. Conclusion: CLA supplementation fails to promote the re-establishment of hepatic lipid metabolism in tumour-bearing animals, and therefore is not recommended in cancer-related cachexia. (C) 2018 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved. |
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Liver lipid metabolism disruption in cancer cachexia is aggravated by cla supplementation -induced inflammationCLACachexiaLiverLipid metabolismInflammationBackground & aims: The liver is the main organ regulating metabolism. In spite of that, few studies examine liver metabolism in cachexia, a wasting syndrome associated with increased morbidity and mortality in cancer. Cachexia induces major metabolic disruption, inflammation and fat and lean mass loss. We have previously shown impairment of hepatic lipid metabolism in cancer cachexia that contributes to the aggravation of the symptoms. The present study addresses the effects of Conjugated Linoleic Acid supplementation upon liver lipid metabolism in cachectic rats. Methods: Male Wistar rats were randomly assigned to control groups (C) receiving 0.9 NaCl (Placebo -CP); or to groups supplemented with sunflower oil (CSF), supplemented with CLA (CCLA), or still, to tumour bearing animals (T) receiving NaCl (TP), sunflower oil (TSF), or CLA (TCLA). Supplementation (0.5 ml) by gavage was carried out for 14 days. Body weight, dietary intake, glucose, cholesterol and triacylglycerol plasma content, liver glycogen and triacylglycerol content and mRNA expression of liver carnitine palmitoyltransferase I and II (CPT I and II), as well as microsomal triglyceride transfer protein (MTP), liver fatty acid-binding protein (L-FABP), peroxisome proliferator-activated receptor-alpha (PPAR-alpha), and apolipoprotein B (apoB), were assessed. Results: Liver CPT II activity was reduced in all groups, when compared with CP. Hepatic mRNA expression of MTP, apoB and FABP was reduced in TCLA, when compared with all groups. TCLA also presented increased hepatic and plasma triacylglycerol content, when compared with all T groups. Adipose tissue-derived inflammatory factors were assessed. No differences among the groups were observed in regard to Retro Peritoneal Adipose Tissue cytokine (IL-1 beta, IL-6, and TNF-alpha) protein content and expression, with the exception of IL-10 in tumour-bearing animals. In the Epididymal Adipose Tissue, the inflammatory cytokines were augmented in TCLA, compared with all other groups. Conclusion: CLA supplementation fails to promote the re-establishment of hepatic lipid metabolism in tumour-bearing animals, and therefore is not recommended in cancer-related cachexia. (C) 2018 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Univ Sao Paulo, Canc Metab Res Grp, Inst Biomed Sci, Sao Paulo, BrazilUniv Sao Paulo, Fac Med, Sao Paulo, BrazilUniv Fed Sao Paulo UNIFESP, Biosci Dept, Campus Baixada Santista, Santos, BrazilUniv Estadual Paulista, Exercise & Immunometab Res Grp, Dept Phys Educ, Presidente Prudente, BrazilSapienza Univ Rome, Dept Clin Med, Rome, ItalyUniv Estadual Paulista, Exercise & Immunometab Res Grp, Dept Phys Educ, Presidente Prudente, BrazilFAPESP: 2012/50079-0Churchill LivingstoneUniversidade de São Paulo (USP)Universidade Federal de São Paulo (UNIFESP)Universidade Estadual Paulista (Unesp)Sapienza Univ RomeGoncalves, Daniela CaetanoLira, Fabio Santos [UNESP]Yamashita, Alex ShimuraCarnevali Junior, Luiz CarlosEder, RobsonLaviano, AlessandroLeite Seelaender, Marilia Cerqueira2020-12-10T19:39:22Z2020-12-10T19:39:22Z2019-10-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article2219-2230http://dx.doi.org/10.1016/j.clnu.2018.09.023Clinical Nutrition. Edinburgh: Churchill Livingstone, v. 38, n. 5, p. 2219-2230, 2019.0261-5614http://hdl.handle.net/11449/19627410.1016/j.clnu.2018.09.023WOS:000492797600031Web of Sciencereponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengClinical Nutritioninfo:eu-repo/semantics/openAccess2024-06-18T17:42:40Zoai:repositorio.unesp.br:11449/196274Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-08-05T14:44:17.449341Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false |
dc.title.none.fl_str_mv |
Liver lipid metabolism disruption in cancer cachexia is aggravated by cla supplementation -induced inflammation |
title |
Liver lipid metabolism disruption in cancer cachexia is aggravated by cla supplementation -induced inflammation |
spellingShingle |
Liver lipid metabolism disruption in cancer cachexia is aggravated by cla supplementation -induced inflammation Goncalves, Daniela Caetano CLA Cachexia Liver Lipid metabolism Inflammation |
title_short |
Liver lipid metabolism disruption in cancer cachexia is aggravated by cla supplementation -induced inflammation |
title_full |
Liver lipid metabolism disruption in cancer cachexia is aggravated by cla supplementation -induced inflammation |
title_fullStr |
Liver lipid metabolism disruption in cancer cachexia is aggravated by cla supplementation -induced inflammation |
title_full_unstemmed |
Liver lipid metabolism disruption in cancer cachexia is aggravated by cla supplementation -induced inflammation |
title_sort |
Liver lipid metabolism disruption in cancer cachexia is aggravated by cla supplementation -induced inflammation |
author |
Goncalves, Daniela Caetano |
author_facet |
Goncalves, Daniela Caetano Lira, Fabio Santos [UNESP] Yamashita, Alex Shimura Carnevali Junior, Luiz Carlos Eder, Robson Laviano, Alessandro Leite Seelaender, Marilia Cerqueira |
author_role |
author |
author2 |
Lira, Fabio Santos [UNESP] Yamashita, Alex Shimura Carnevali Junior, Luiz Carlos Eder, Robson Laviano, Alessandro Leite Seelaender, Marilia Cerqueira |
author2_role |
author author author author author author |
dc.contributor.none.fl_str_mv |
Universidade de São Paulo (USP) Universidade Federal de São Paulo (UNIFESP) Universidade Estadual Paulista (Unesp) Sapienza Univ Rome |
dc.contributor.author.fl_str_mv |
Goncalves, Daniela Caetano Lira, Fabio Santos [UNESP] Yamashita, Alex Shimura Carnevali Junior, Luiz Carlos Eder, Robson Laviano, Alessandro Leite Seelaender, Marilia Cerqueira |
dc.subject.por.fl_str_mv |
CLA Cachexia Liver Lipid metabolism Inflammation |
topic |
CLA Cachexia Liver Lipid metabolism Inflammation |
description |
Background & aims: The liver is the main organ regulating metabolism. In spite of that, few studies examine liver metabolism in cachexia, a wasting syndrome associated with increased morbidity and mortality in cancer. Cachexia induces major metabolic disruption, inflammation and fat and lean mass loss. We have previously shown impairment of hepatic lipid metabolism in cancer cachexia that contributes to the aggravation of the symptoms. The present study addresses the effects of Conjugated Linoleic Acid supplementation upon liver lipid metabolism in cachectic rats. Methods: Male Wistar rats were randomly assigned to control groups (C) receiving 0.9 NaCl (Placebo -CP); or to groups supplemented with sunflower oil (CSF), supplemented with CLA (CCLA), or still, to tumour bearing animals (T) receiving NaCl (TP), sunflower oil (TSF), or CLA (TCLA). Supplementation (0.5 ml) by gavage was carried out for 14 days. Body weight, dietary intake, glucose, cholesterol and triacylglycerol plasma content, liver glycogen and triacylglycerol content and mRNA expression of liver carnitine palmitoyltransferase I and II (CPT I and II), as well as microsomal triglyceride transfer protein (MTP), liver fatty acid-binding protein (L-FABP), peroxisome proliferator-activated receptor-alpha (PPAR-alpha), and apolipoprotein B (apoB), were assessed. Results: Liver CPT II activity was reduced in all groups, when compared with CP. Hepatic mRNA expression of MTP, apoB and FABP was reduced in TCLA, when compared with all groups. TCLA also presented increased hepatic and plasma triacylglycerol content, when compared with all T groups. Adipose tissue-derived inflammatory factors were assessed. No differences among the groups were observed in regard to Retro Peritoneal Adipose Tissue cytokine (IL-1 beta, IL-6, and TNF-alpha) protein content and expression, with the exception of IL-10 in tumour-bearing animals. In the Epididymal Adipose Tissue, the inflammatory cytokines were augmented in TCLA, compared with all other groups. Conclusion: CLA supplementation fails to promote the re-establishment of hepatic lipid metabolism in tumour-bearing animals, and therefore is not recommended in cancer-related cachexia. (C) 2018 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved. |
publishDate |
2019 |
dc.date.none.fl_str_mv |
2019-10-01 2020-12-10T19:39:22Z 2020-12-10T19:39:22Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://dx.doi.org/10.1016/j.clnu.2018.09.023 Clinical Nutrition. Edinburgh: Churchill Livingstone, v. 38, n. 5, p. 2219-2230, 2019. 0261-5614 http://hdl.handle.net/11449/196274 10.1016/j.clnu.2018.09.023 WOS:000492797600031 |
url |
http://dx.doi.org/10.1016/j.clnu.2018.09.023 http://hdl.handle.net/11449/196274 |
identifier_str_mv |
Clinical Nutrition. Edinburgh: Churchill Livingstone, v. 38, n. 5, p. 2219-2230, 2019. 0261-5614 10.1016/j.clnu.2018.09.023 WOS:000492797600031 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Clinical Nutrition |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
2219-2230 |
dc.publisher.none.fl_str_mv |
Churchill Livingstone |
publisher.none.fl_str_mv |
Churchill Livingstone |
dc.source.none.fl_str_mv |
Web of Science reponame:Repositório Institucional da UNESP instname:Universidade Estadual Paulista (UNESP) instacron:UNESP |
instname_str |
Universidade Estadual Paulista (UNESP) |
instacron_str |
UNESP |
institution |
UNESP |
reponame_str |
Repositório Institucional da UNESP |
collection |
Repositório Institucional da UNESP |
repository.name.fl_str_mv |
Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP) |
repository.mail.fl_str_mv |
|
_version_ |
1808128410627604480 |