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

被引:61
作者
Martins, Amanda R. [1 ]
Crisma, Amanda R. [1 ]
Masi, Laureane N. [2 ]
Amaral, Catia L. [1 ,3 ]
Marzuca-Nassr, Gabriel N. [1 ,4 ]
Bomfim, Lucas H. M. [5 ]
Teodoro, Bruno G. [6 ]
Queiroz, Andre L. [6 ]
Serdan, Tamires D. A. [2 ]
Torres, Rosangela P. [7 ]
Mancini-Filho, Jorge [7 ]
Rodrigues, Alice C. [1 ]
Alba-Loureiro, Tatiana C. [1 ]
Pithon-Curi, Tania C. [2 ]
Gorjao, Renata [2 ]
Silveira, Leonardo R. [5 ]
Curi, Rui [1 ,2 ]
Newsholme, Philip [8 ]
Hirabara, Sandro M. [1 ,2 ]
机构
[1] Univ Sao Paulo, Inst Biomed Sci, Sao Paulo, Brazil
[2] Cruzeiro do Sul Univ, Inst Phys Act Sci & Sports, Sao Paulo, Brazil
[3] State Univ Goias, Exact & Technol Sci, Anapolis, Go, Brazil
[4] Univ La Frontera, Fac Med, Dept Internal Med, Temuco, Chile
[5] Univ Estadual Campinas, Inst Biol, Campinas, SP, Brazil
[6] Univ Sao Paulo, Dept Biochem & Immunol, Fac Med, Ribeirao Preto, Brazil
[7] Univ Sao Paulo, Fac Pharmaceut Sci, Sao Paulo, Brazil
[8] Curtin Univ, Curtin Hlth Innovat Res Inst, Sch Biomed Sci, Perth, WA 6152, Australia
基金
巴西圣保罗研究基金会;
关键词
Insulin resistance; Fish oil; Skeletal muscle; Mitochondrial function; Obesity; ACTIVATED PROTEIN-KINASE; ADIPOSE-TISSUE INFLAMMATION; OXIDATIVE STRESS; SOLEUS MUSCLE; RECEPTOR-ALPHA; GLYCOGEN-SYNTHESIS; LIPID-METABOLISM; DIABETIC MICE; LINOLEIC-ACID; KNOCKOUT MICE;
D O I
10.1016/j.jnutbio.2017.11.012
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:76 / 88
页数:13
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