Attenuation of obesity and insulin resistance by fish oil supplementation is associated with improved skeletal muscle mitochondrial function in mice fed a high-fat diet

Primer Autor
Hirabara, Sandro M.
Co-autores
Martins, Amanda R.#Crisma, Amanda R.#Masi, Laureane N.#Amaral, Catia L.#Marzuca-Nassr, Gabriel N.#Bomfim, Lucas H. M.#Teodoro, Bruno G.#Queiroz, Andre L.#Serdan, Tamires D. A.#Torres, Rosangela P.#Mancini-Filho, Jorge#Rodrigues, Alice C.#Alba-Loureiro, Tatiana C.#Pithon-Curi, Tania C.#Gorjao, Renata#Silveira, Leonardo R.#Curi, Rui#Newsholme, Philip
Título
Attenuation of obesity and insulin resistance by fish oil supplementation is associated with improved skeletal muscle mitochondrial function in mice fed a high-fat diet
Editorial
ELSEVIER SCIENCE INC
Revista
JOURNAL OF NUTRITIONAL BIOCHEMISTRY
Lenguaje
en
Resumen
Omega-3 polyunsaturated fatty acids (n-3 PUFAs) have been reported to improve insulin sensitivity and glucose homeostasis in animal models of insulin resistance, but the involved mechanisms still remain unresolved. In this study, we evaluated the effects of fish oil (FO), a source of n-3 PUFAs, on obesity, insulin resistance and muscle mitochondrial function in mice fed a high-fat diet (HFD). C57B1/6 male mice, 8 weeks old, were divided into four groups: control diet (C), high-fat diet (H), C+FO (CFO) and H+FO (HFO). FO was administered by oral gavage (2 g/kg b.w.), three times a week, starting 4 weeks before diet administration until the end of the experimental protocol. HFD-induced obesity and insulin resistance associated with impaired skeletal muscle mitochondrial function, as indicated by decreased oxygen consumption, tricarboxylic acid cycle intermediate (TCAi) contents (citrate, alpha-ketoglutarate, malate and oxaloacetate), oxidative phosphorylation protein content and mitochondrial biogenesis. These effects were associated with elevated reactive oxygen species production, decreased PGC1-a transcription and reduced Akt phosphorylation. The changes induced by the HFD were partially attenuated by FO, which decreased obesity and insulin resistance and increased mitochondria] function. In the H group, FO supplementation also improved oxygen consumption, increased TCAi content, and Akt and AMPK phosphorylation, and up-regulated mRNA expression of Gpat1, Pepck, catalase and mitochondrial proteins (Pgc1 alpha, Ppar alpha, Cpt1 and Ucp3). These results suggest that dietary FO attenuates the deleterious effects of the HFD (obesity and insulin resistance) by improving skeletal muscle mitochondrial function. (C) 2017 Elsevier Inc. All rights reserved.
Tipo de Recurso
Artículo original
Description
FAPESP, CNPq, CAPES, and Guggenheim Foundation supported this study. PN received FAPESP travel support and is grateful to the Curtin University School of Biomedical Sciences for research support. Authors are grateful for the technical assistance from Dr. Gilson Masahiro Murata and Mr. Jose Roberto Mendonca.
doi
10.1016/j.jnutbio.2017.11.012
Formato Recurso
pdf
Palabras Claves
Insulin resistance# Fish oil# Skeletal muscle# Mitochondrial function# Obesity
Insulin resistance# Fish oil# Skeletal muscle# Mitochondrial function# Obesity
Ubicación del archivo
http://dx.doi.org/10.1016/j.jnutbio.2017.11.012
Categoría OCDE
Biochemistry & Molecular Biology# Nutrition & Dietetics
Materias
Resistencia a la insulina# Aceite de pescado# Músculo esquelético# Función mitocondrial# Obesidad
Resistencia a la insulina# Aceite de pescado# Músculo esquelético# Función mitocondrial# Obesidad
Id de Web of Science
WOS:000432416000008
Título de la cita (Recomendado-único)
Attenuation of obesity and insulin resistance by fish oil supplementation is associated with improved skeletal muscle mitochondrial function in mice fed a high-fat diet
Identificador del recurso (Mandatado-único)
Artículo original
Versión del recurso (Recomendado-único)
version publicada
Editorial
ELSEVIER SCIENCE INC
Revista/Libro
JOURNAL OF NUTRITIONAL BIOCHEMISTRY
Categoría WOS
Bioquímica y Biología Molecular# Nutrición y Dietética
ISSN
0955-2863
Idioma
en
Referencia del Financiador (Mandatado si es aplicable-repetible)
FAPESP#CNPq#CAPES
Descripción
FAPESP, CNPq, CAPES, and Guggenheim Foundation supported this study. PN received FAPESP travel support and is grateful to the Curtin University School of Biomedical Sciences for research support. Authors are grateful for the technical assistance from Dr. Gilson Masahiro Murata and Mr. Jose Roberto Mendonca.
Formato
pdf
Tipo de ruta
hibrida#verde
Access Rights
metadata
Derechos de acceso
metadata
Página de inicio (Recomendado-único)
780
Página final (Recomendado-único)
784
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