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Liver lipid metabolism disruption in cancer cachexia is aggravated by cla supplementation -induced inflammation.
Clin Nutr. 2019 10; 38(5):2219-2230.CN

Abstract

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-1β, IL-6, and TNF-α) 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.

Authors+Show Affiliations

Cancer Metabolism Research Group, Institute of Biomedical Sciences and Faculdade de Medicina, University of São Paulo, São Paulo, Brazil; Biosciences Department, Universidade Federal de São Paulo (UNIFESP), Campus Baixada Santista, Santos, Brazil.Exercise and Immunometabolism Research Group, Department of Physical Education, Universidade Estadual Paulista, Presidente Prudente, Brazil.Cancer Metabolism Research Group, Institute of Biomedical Sciences and Faculdade de Medicina, University of São Paulo, São Paulo, Brazil.Cancer Metabolism Research Group, Institute of Biomedical Sciences and Faculdade de Medicina, University of São Paulo, São Paulo, Brazil.Cancer Metabolism Research Group, Institute of Biomedical Sciences and Faculdade de Medicina, University of São Paulo, São Paulo, Brazil.Department of Clinical Medicine, Sapienza University of Rome, Italy.Cancer Metabolism Research Group, Institute of Biomedical Sciences and Faculdade de Medicina, University of São Paulo, São Paulo, Brazil. Electronic address: seelaend@icb.usp.br.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

30322784

Citation

Gonçalves, Daniela Caetano, et al. "Liver Lipid Metabolism Disruption in Cancer Cachexia Is Aggravated By Cla Supplementation -induced Inflammation." Clinical Nutrition (Edinburgh, Scotland), vol. 38, no. 5, 2019, pp. 2219-2230.
Gonçalves DC, Lira FS, Yamashita AS, et al. Liver lipid metabolism disruption in cancer cachexia is aggravated by cla supplementation -induced inflammation. Clin Nutr. 2019;38(5):2219-2230.
Gonçalves, D. C., Lira, F. S., Yamashita, A. S., Carnevali Junior, L. C., Eder, R., Laviano, A., & Seelaender, M. C. L. (2019). Liver lipid metabolism disruption in cancer cachexia is aggravated by cla supplementation -induced inflammation. Clinical Nutrition (Edinburgh, Scotland), 38(5), 2219-2230. https://doi.org/10.1016/j.clnu.2018.09.023
Gonçalves DC, et al. Liver Lipid Metabolism Disruption in Cancer Cachexia Is Aggravated By Cla Supplementation -induced Inflammation. Clin Nutr. 2019;38(5):2219-2230. PubMed PMID: 30322784.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Liver lipid metabolism disruption in cancer cachexia is aggravated by cla supplementation -induced inflammation. AU - Gonçalves,Daniela Caetano, AU - Lira,Fábio Santos, AU - Yamashita,Alex Shimura, AU - Carnevali Junior,Luiz Carlos, AU - Eder,Robson, AU - Laviano,Alessandro, AU - Seelaender,Marília Cerqueira Leite, Y1 - 2018/09/25/ PY - 2015/10/27/received PY - 2018/09/15/revised PY - 2018/09/18/accepted PY - 2018/10/17/pubmed PY - 2020/9/9/medline PY - 2018/10/17/entrez KW - CLA KW - Cachexia KW - Inflammation KW - Lipid metabolism KW - Liver SP - 2219 EP - 2230 JF - Clinical nutrition (Edinburgh, Scotland) JO - Clin Nutr VL - 38 IS - 5 N2 - 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-1β, IL-6, and TNF-α) 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. SN - 1532-1983 UR - https://www.unboundmedicine.com/medline/citation/30322784/Liver_lipid_metabolism_disruption_in_cancer_cachexia_is_aggravated_by_cla_supplementation__induced_inflammation_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0261-5614(18)32461-0 DB - PRIME DP - Unbound Medicine ER -