首页> 外文期刊>The British Journal of Nutrition >Effects of eicosapentaenoic acid ethyl ester on visfatin and apelin in lean and overweight (cafeteria diet-fed) rats
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Effects of eicosapentaenoic acid ethyl ester on visfatin and apelin in lean and overweight (cafeteria diet-fed) rats

机译:二十碳五烯酸乙酯对瘦肉和超重(食堂饮食喂养)大鼠visfatin和apelin的影响

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Previous studies have demonstrated that the n-3 fatty acid EPA improves insulin resistance induced by high-fat diets. The aim of the present study was to investigate the potential role of visfatin and apelin in the insulin-sensitising effects of EPA ethyl ester. The effects of EPA on muscle and adipose GLUT mRNA, as well as on liver glucokinase (GK) and glucose-6-phosphatase (G6Pase) activity, were investigated. Male Wistar rats fed on a standard diet or a high-fat cafeteria diet were daily treated by oral administration with EPA ethyl ester (1 g/kg) for 5 weeks. A significant decrease (P < 0.01) in white adipose tissue (WAT) visfatin mRNA levels was found in the cafeteria-fed rats, which was reversed by EPA administration (P < 0.05). Moreover, a negative relationship was observed between homeostatic model assessment (HOMA) and the visfatin:total WAT ratio. In contrast, cafeteria-diet feeding caused a significant increase (P < 0.01) in apelin mRNA in visceral WAT. EPA increased (P < 0.01) apelin gene expression, and a negative relationship between HOMA index with visceral apelin mRNA and serum apelin:total WAT ratio was also observed. EPA treatment did not induce changes in skeletal muscle GLUT1, GLUT4 or insulin receptor mRNA levels. Neither liver GK and G6Pase activity nor the GK:G6Pase ratio was modified by EPA. These data suggest that somehow the insulin-sensitising effects of EPA could be related to its stimulatory action on both visfatin and apelin gene expression in visceral fat, while changes in skeletal muscle GLUT, as well as in hepatic glucose production, are not likely to be the main contributing factors in the improvement in insulin resistance induced by EPA.
机译:先前的研究表明,n-3脂肪酸EPA可以改善高脂饮食诱导的胰岛素抵抗。本研究的目的是研究visfatin和apelin在EPA乙酯的胰岛素增敏作用中的潜在作用。研究了EPA对肌肉和脂肪GLUT mRNA的影响,以及对肝脏葡萄糖激酶(GK)和葡萄糖6磷酸酶(G6Pase)活性的影响。以标准饮食或高脂食堂饮食喂养的雄性Wistar大鼠每天通过口服EPA乙酯(1 g / kg)治疗5周。在自助食堂喂养的大鼠中发现白色脂肪组织(WAT)visfatin mRNA水平显着降低(P <0.01),而通过EPA给药可以逆转(P <0.05)。此外,在稳态模型评估(HOMA)与visfatin:WAT总比之间存在负相关关系。相比之下,食堂饮食喂养在内脏WAT中使apelin mRNA显着增加(P <0.01)。 EPA增加(P <0.01)apelin基因表达,并且还观察到HOMA指数与内脏apelin mRNA和血清apelin:总WAT比之间呈负相关。 EPA处理不会引起骨骼肌GLUT1,GLUT4或胰岛素受体mRNA水平的变化。 EPA既不改变肝脏的GK和G6Pase活性,也不改变GK:G6Pase的比例。这些数据表明,某种程度上,EPA的胰岛素增敏作用可能与其对内脏脂肪中的visfatin和apelin基因表达的刺激作用有关,而骨骼肌GLUT的变化以及肝葡萄糖的产生则不太可能。 EPA引起胰岛素抵抗改善的主要因素。

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