首页> 外文期刊>Journal of Lipid Research >Dietary n-3 PUFA deprivation for 15 weeks upregulates elongase and desaturase expression in rat liver but not brain
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Dietary n-3 PUFA deprivation for 15 weeks upregulates elongase and desaturase expression in rat liver but not brain

机译:饮食中的n-3 PUFA剥夺15周可上调大鼠肝脏而非大脑中的延伸酶和去饱和酶表达

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Fifteen weeks of dietary n-3 PUFA deprivation increases coefficients of conversion of circulating alpha-linolenic acid (alpha-LNA; 18:3n-3) to docosahexaenoic acid ( DHA; 22:6n-3) in rat liver but not brain. To determine whether these increases reflect organ differences in enzymatic activities, we examined brain and liver expression of converting enzymes and of two of their transcription factors, peroxisome proliferator-activated receptor a ( PPAR alpha) and sterol-regulatory element binding protein-1 (SREBP-1), in rats fed an n-3 PUFA "adequate" ( 4.6% alpha-LNA of total fatty acid, no DHA) or "deficient" ( 0.2% alpha-LNA, no DHA) diet for 15 weeks after weaning. In rats fed the deficient compared with the adequate diet, mRNA and activity levels of Delta 5 and Delta 6 desaturases and elongases 2 and 5 were upregulated in liver but not brain, but liver PPAR alpha and SREBP-1 mRNA levels were unchanged. In rats fed the adequate diet, enzyme activities generally were higher in liver than brain. Thus, differences in conversion enzyme expression explain why the liver has a greater capacity to synthesize DHA from circulating alpha-LNA than does the brain in animals on an adequate n-3 PUFA diet and why liver synthesis capacity is increased by dietary deprivation. These data suggest that liver n-3 PUFA metabolism determines DHA availability to the brain when DHA is absent from the diet.
机译:饮食中n-3 PUFA缺乏15周会增加大鼠肝脏而非大脑中循环中的α-亚麻酸(α-LNA; 18:3n-3)转化为二十二碳六烯酸(DHA; 22:6n-3)的转化系数。为了确定这些增加是否反映了酶活性的器官差异,我们检查了大脑和肝脏中转化酶及其两种转录因子,过氧化物酶体增殖物激活受体a(PPARα)和固醇调节元件结合蛋白1(SREBP)的表达-1),在断奶后15周内,喂食n-3 PUFA“足够”(总脂肪酸的4.6%α-LNA,无DHA)或“缺乏”(0.2%α-LNA,无DHA)的大鼠。与充足饮食相比,在进食不足的大鼠中,肝脏而非大脑中的Delta 5和Delta 6去饱和酶以及延伸酶2和5的mRNA和活性水平上调,但肝脏PPARα和SREBP-1 mRNA水平没有变化。在饮食充足的大鼠中,肝脏中的酶活性通常高于大脑。因此,转化酶表达的差异解释了为什么肝脏具有足够的循环α-LNA合成DHA的能力,而不是动物在充足的n-3 PUFA饮食下的大脑合成能力,以及为什么饮食缺乏会增加肝脏的合成能力。这些数据表明,当饮食中不含DHA时,肝脏n-3 PUFA代谢决定了大脑中DHA的利用率。

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