Liver lipid metabolism disruption in cancer cachexia is aggravated by cla supplementation -induced inflammation

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dc.contributor.authorGoncalves, Daniela Caetano
dc.contributor.authorLira, Fabio Santos [UNESP]
dc.contributor.authorYamashita, Alex Shimura
dc.contributor.authorCarnevali Junior, Luiz Carlos
dc.contributor.authorEder, Robson
dc.contributor.authorLaviano, Alessandro
dc.contributor.authorLeite Seelaender, Marilia Cerqueira
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionSapienza Univ Rome
dc.date.accessioned2020-12-10T19:39:22Z
dc.date.available2020-12-10T19:39:22Z
dc.date.issued2019-10-01
dc.description.abstractBackground & 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.en
dc.description.affiliationUniv Sao Paulo, Canc Metab Res Grp, Inst Biomed Sci, Sao Paulo, Brazil
dc.description.affiliationUniv Sao Paulo, Fac Med, Sao Paulo, Brazil
dc.description.affiliationUniv Fed Sao Paulo UNIFESP, Biosci Dept, Campus Baixada Santista, Santos, Brazil
dc.description.affiliationUniv Estadual Paulista, Exercise & Immunometab Res Grp, Dept Phys Educ, Presidente Prudente, Brazil
dc.description.affiliationSapienza Univ Rome, Dept Clin Med, Rome, Italy
dc.description.affiliationUnespUniv Estadual Paulista, Exercise & Immunometab Res Grp, Dept Phys Educ, Presidente Prudente, Brazil
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipIdFAPESP: 2012/50079-0
dc.format.extent2219-2230
dc.identifierhttp://dx.doi.org/10.1016/j.clnu.2018.09.023
dc.identifier.citationClinical Nutrition. Edinburgh: Churchill Livingstone, v. 38, n. 5, p. 2219-2230, 2019.
dc.identifier.doi10.1016/j.clnu.2018.09.023
dc.identifier.issn0261-5614
dc.identifier.urihttp://hdl.handle.net/11449/196274
dc.identifier.wosWOS:000492797600031
dc.language.isoeng
dc.publisherChurchill Livingstone
dc.relation.ispartofClinical Nutrition
dc.sourceWeb of Science
dc.subjectCLA
dc.subjectCachexia
dc.subjectLiver
dc.subjectLipid metabolism
dc.subjectInflammation
dc.titleLiver lipid metabolism disruption in cancer cachexia is aggravated by cla supplementation -induced inflammationen
dc.typeArtigo
dcterms.rightsHolderChurchill Livingstone
unesp.author.orcid0000-0002-9999-8020[7]

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