The Dietary Replacement of Soybean Oil by Canola Oil Does Not Prevent Liver Fatty Acid Accumulation and Liver Inflammation in Mice

Autor(es)

Antunes, Marina Masetto ^[1] ; Godoy, Guilherme ^[1] ; Fernandes, Ingrid de Lima ^[2] ; Manin, Luciana Pelissari ^[2] ; Zappielo, Caroline ^[2] ; Masi, Laureane Nunes ^[3] ; Barbosa de Oliveira, Vivian Araujo ^[3] ; Visentainer, Jesui Vergilio ^[2] ; Curi, Rui ^[3] ; Bazotte, Roberto Barbosa ^[1]

Afiliação do(s) autor(es)

^[1] Univ Estadual Maringa, Dept Pharmacol & Therapeut, BR-87020900 Maringa, Parana - Brazil

^[2] Univ Estadual Maringa, Dept Chem, BR-87020900 Maringa, Parana - Brazil

^[3] Cruzeiro do Sul Univ, Interdisciplinary Postgrad Program Hlth Sci, BR-03342000 Sao Paulo - Brazil

• Tipo de documento: Artigo Científico
• Fonte: NUTRIENTS; v. 12, n. 12 DEC 2020.
• Citações Web of Science: 2

Resumo

A high-carbohydrate diet (HCD) is a well-established experimental model of accelerated liver fatty acid (FA) deposition and inflammation. In this study, we evaluated whether canola oil can prevent these physiopathological changes. We evaluated hepatic FA accumulation and inflammation in mice fed with a HCD (72.1% carbohydrates) and either canola oil (C group) or soybean oil (S group) as a lipid source for 0, 7, 14, 28, or 56 days. Liver FA compositions were analyzed by gas chromatography. The mRNA expression of acetyl-CoA carboxylase 1 (ACC1) was measured as an indicator of lipogenesis. The mRNA expression of F4/80, tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1 beta, IL-6, and IL-10, as mediators of liver inflammation, were also measured. The C group stored less n-6 polyunsaturated FAs (n-6 PUFAs) and had more intense lipid deposition of monounsaturated FAs (MUFAs), n-3 PUFAs, and total FAs. The C group also showed higher ACC1 expression. Moreover, on day 56, the C group showed higher expressions of the inflammatory genes F4/80, TNF-alpha, IL-1 beta, and IL-6, as well as the anti-inflammatory IL-10. In conclusion, a diet containing canola oil as a lipid source does not prevent the fatty acid accumulation and inflammation induced by a HCD. (AU)

• Processo FAPESP: 18/09868-7 - Mecanismos celulares e moleculares envolvidos na resistência à insulina e inflamação em ratos Wistar obesos e Goto-Kakizaki magros: causas e associações com dieta e exercício físico
• Beneficiário: Rui Curi
• Modalidade de apoio: Auxílio à Pesquisa - Temático