Metabolic and Cardiovascular Diseases Laboratory, Alberta Institute for Human Nutrition, 4-10 Agriculture Forestry Centre, University of Alberta, Edmonton, AB, Canada T6G 2P5.
Br J Nutr. 2011 Jun;105(11):1572-82. doi: 10.1017/S0007114510005453. Epub 2011 Jan 31.
There is increasing interest in the potential chronic beneficial effects of dietary n-3 PUFA on the metabolic syndrome (MetS) and associated cardiovascular complications. We have recently established that increased dietary n-3 PUFA has a profound acute benefit on fasting lipids and the postprandial pro-inflammatory response in the JCR:LA-cp rat, a model of the MetS. However, it is unclear to what extent chronic dietary n-3 PUFA intervention can modulate the progression of end-stage metabolic and vascular complications. The present study aimed to determine the chronic effects of dietary n-3 PUFA supplementation on fasting and non-fasting dyslipidaemia, insulin resistance and vascular complications in the JCR:LA-cp rodent model. JCR:LA-cp rats were fed an isoenergetic lipid-balanced diet supplemented with 5 % n-3 PUFA (w/w) of the total fat (fish oil-derived EPA/DHA) for 16 weeks. Fasting and non-fasting (postprandial) plasma lipid profile was assessed. Hepatic and adipose tissue was probed for the expression of lipogenic proteins (acyl-CoA carboxylase (ACC), fatty acid synthase (FAS) and sterol regulatory element-binding protein-1 (SREBP-1)), while the activity of Jun N-terminal kinase (JNK) was assessed via Western blot to target phosphorylated JNK protein in primary enterocytes. The frequency of myocardial lesions was assessed by haematoxylin and eosin staining. Increased dietary n-3 PUFA improved both the fasting and postprandial lipid profiles (TAG, cholesterol and apoB48) in the JCR:LA-cp rat, potentially via the down-regulation of the hepatic or adipose tissue expression of lipogenic enzymes (ACC, FAS and SREBP-1). Rats fed the 5 % n-3 PUFA diet had lower (58·2 %; P < 0·01) enterocytic phosphorylated JNK protein and secreted less cholesterol (30 %; P < 0·05) into mesenteric lymph compared with the control. The chronic metabolic benefits of dietary n-3 PUFA may underlie the potential to reduce vascular complications during the MetS, including the observed reduction in the frequency (approximately 80 %) of late-stage 3 myocardial lesions.
人们对饮食中 n-3PUFA 对代谢综合征(MetS)及其相关心血管并发症的潜在慢性有益影响越来越感兴趣。我们最近发现,增加饮食中 n-3PUFA 对 JCR:LA-cp 大鼠(MetS 的模型)的空腹脂质和餐后促炎反应有深远的急性益处。然而,尚不清楚慢性饮食 n-3PUFA 干预在多大程度上可以调节终末期代谢和血管并发症的进展。本研究旨在确定饮食中 n-3PUFA 补充对 JCR:LA-cp 啮齿动物模型的空腹和非空腹血脂异常、胰岛素抵抗和血管并发症的慢性影响。JCR:LA-cp 大鼠喂食等能量脂质平衡饮食,其中总脂肪(来自鱼油的 EPA/DHA)的 5%为 n-3PUFA(w/w),持续 16 周。评估空腹和非空腹(餐后)血浆脂质谱。研究了肝和脂肪组织中脂肪生成蛋白(酰基辅酶 A 羧化酶(ACC)、脂肪酸合酶(FAS)和固醇调节元件结合蛋白-1(SREBP-1))的表达,同时通过 Western blot 评估 Jun N-末端激酶(JNK)的活性,以靶向原代肠细胞中磷酸化的 JNK 蛋白。通过苏木精和伊红染色评估心肌病变的频率。增加饮食中 n-3PUFA 改善了 JCR:LA-cp 大鼠的空腹和餐后脂质谱(TAG、胆固醇和 apoB48),可能是通过下调肝或脂肪组织中脂肪生成酶(ACC、FAS 和 SREBP-1)的表达。与对照组相比,喂食 5%n-3PUFA 饮食的大鼠肠细胞中磷酸化 JNK 蛋白水平降低(58.2%;P<0.01),且分泌到肠系膜淋巴中的胆固醇减少(30%;P<0.05)。饮食中 n-3PUFA 的慢性代谢益处可能是降低 MetS 期间血管并发症的潜在基础,包括观察到晚期 3 期心肌病变的频率降低(约 80%)。