The combination of conjugated linoleic acid (CLA) and extra virgin olive oil increases mitochondrial and body metabolism and prevents CLA-associated insulin resistance and liver hypertrophy in C57B1/6 mice

Autor(es)

Baraldi, Flavia G. ^[1] ; Vicentini, Tatiane M. ^[1] ; Teodoro, Bruno G. ^[1] ; Dalalio, Felipe M. ^[1] ; Dechandt, Carlos R. P. ^[1] ; Prado, Ieda M. R. ^[1] ; Curti, Carlos ^[1] ; Cardoso, Fernanda C. ^[2] ; Uyemura, Sergio A. ^[2] ; Alberici, Luciane C. ^[1]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Fac Ciencias Farmaceut & Ribeirao Preto, Dept Fis & Quim, Av Cafe S-N, BR-14040903 Ribeirao Preto, SP - Brazil

^[2] Univ Sao Paulo, Fac Ciencias Farmaceut & Ribeirao Preto, Dept Anal Clin Toxicol & Bromatol, Av Cafe S-N, BR-14040903 Ribeirao Preto, SP - Brazil

• Tipo de documento: Artigo Científico
• Fonte: JOURNAL OF NUTRITIONAL BIOCHEMISTRY; v. 28, p. 147-154, FEB 2016.
• Citações Web of Science: 7

Resumo

Clinical conditions associated with obesity can be improved by daily intake of conjugated linoleic acid (CLA) or extra virgin olive oil (EVOO). Here we investigated whether dietary supplementation with CLA and EVOO, either alone or in combination, changes body metabolism associated with mitochondrial energetics. Male C57B1/6 mice were divided into one of four groups: CLA (1:1 cis-9, trans-11:trans-10, cis-12; 18:2 isomers), EVOO, CLA plus EV00 or control (linoleic acid). Each mouse received 3 g/kg body weight of the stated oil by gavage on alternating days for 60 days. Dietary supplementation with CIA, alone or in combination with EVOO: (a) reduced the white adipose tissue gain; (b) increased body VO2 consumption, VCO2 production and energy expenditure; (c) elevated uncoupling protein (UCP)-2 expression and UCP activity in isolated liver mitochondria. This organelle, when energized with NAD+-linked substrates, produced high amounts of H2O2 without inducing oxidative damage. Dietary supplementation with EVOO alone did not change any metabolic parameter, but supplementation with CIA itself promoted insulin resistance and elevated weight, lipid content and acetyl-CoA carboxylase-1 expression in liver. Interestingly, the in vivo antioxidant therapy with N-acetylcysteine abolished the CIA-induced rise of body metabolism and liver UCP expression and activity, while the in vitro antioxidant treatment with catalase mitigated the CIA-dependent UCP-2 expression in hepatocytes; these findings suggest the participation of an oxidative dependent pathway. Therefore, this study clarifies the mechanisms by which CIA induces liver UCP expression and activity, and demonstrates for the first time the beneficial effects of combined CIA and EV00 supplementation. (C) 2015 Elsevier Inc. All rights reserved. (AU)

• Processo FAPESP: 10/17259-9 - Estudos sobre mecanismos de desacoplamento mitocondriais por ácidos graxos não-esterificados como estratégia de prevenção/tratamento da obesidade
• Beneficiário: Luciane Carla Alberici
• Modalidade de apoio: Auxílio à Pesquisa - Jovens Pesquisadores