Manifestations of fasting-induced fatty liver and rapid recovery from steatosis in voles fed lard or flaxseed oil lipids.

Manifestations of fasting-induced fatty liver and rapid recovery from steatosis in voles fed lard or flaxseed oil lipids.
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DOI:
10.3390/nu5104211
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发表时间:
2013-10-22
期刊:
影响因子:
5.9
通讯作者:
Nieminen P
Nieminen P
中科院分区:
医学2区
文献类型:
--
作者:
Mustonen AM;Kärjä V;Kilpiö M;Tammi R;Tammi M;Rouvinen-Watt K;Halonen T;Nieminen P

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长链n-3多不饱和脂肪酸(PUFA)对脂肪沉积、心血管疾病和肝脏脂肪变性具有有益作用。我们调查了如何饮食的基础上猪油(主要是饱和和单不饱和脂肪酸)或亚麻籽油(富含18:3 n-3)影响肝脏脂肪-%和脂肪酸配置文件的苔原田鼠(Microtus oeconomus)。我们还研究了透明质酸(HA)在脂肪肝病理学中的潜在参与,以及禁食诱导的脂肪变性的发展和恢复是否受到n-3 PUFA的影响。膳食脂肪酸组成表现在肝脏脂肪酸特征中。禁食18小时诱导大泡性脂肪变性,肝脏脂肪%增加至22%,与之前的饮食无关。禁食诱导的脂肪变性不涉及炎症或结缔组织活化,这表明白细胞蓄积和HA增加均不存在。食物剥夺改变了肝脏脂肪酸的特征,使其更接近饮食。禁食降低了长链n-3 PUFA的比例在两种饮食制度和n-3/n-6 PUFA的比例在猪油喂养的田鼠。长链n-3 PUFA的减少可能通过调节脂质代谢基因的表达促进脂质蓄积。日粮18:3 n-3不能阻止禁食田鼠脂肪变性的发展或减轻其表现,也不能促进其恢复。
Long-chain n-3 polyunsaturated fatty acids (PUFA) can have beneficial effects against fat deposition, cardiovascular diseases, and liver steatosis. We investigated how diets based on lard (predominantly saturated and monounsaturated fatty acids) or flaxseed oil (rich in 18:3n-3) affect liver fat-% and fatty acid profiles of tundra voles (Microtus oeconomus). We also studied potential participation of hyaluronan (HA) in the pathology of fatty liver and whether the development and recovery of fasting-induced steatosis are influenced by n-3 PUFA. The dietary fatty acid composition was manifested in the liver fatty acid signatures. Fasting for 18 h induced macrovesicular steatosis and the liver fat-% increased to 22% independent of the preceding diet. Fasting-induced steatosis did not involve inflammation or connective tissue activation indicated by the absence of both leukocyte accumulation and increased HA. Food deprivation modified the liver fatty acid signatures to resemble more closely the diets. Fasting reduced the proportions of long-chain n-3 PUFA in both dietary regimes and n-3/n-6 PUFA ratios in the lard-fed voles. Decreases in long-chain n-3 PUFA may promote lipid accumulation by modulating the expression of lipid-metabolizing genes. Dietary 18:3n-3 did not prevent the development or attenuate the manifestation of steatosis in the fasted voles or promote the recovery.
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