必需脂肪酸缺乏大鼠非寒战产热及褐色脂肪组织活性。

M Goubern, J Yazbeck, C Senault, R Portet
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引用次数: 7

摘要

研究了必需脂肪酸(EFA)缺乏对冷驯化大鼠能量代谢和肩胛间棕色脂肪组织(BAT)活性的影响。断奶雄性Long-Evans大鼠饲喂低脂半纯化饲料(对照饲料,2%葵花籽油;缺乏脂肪酸的饮食,2%氢化椰子油),持续9周。在过去的5周里,他们一直暴露在5摄氏度的环境中。在EFA缺乏的大鼠中,与对照组相比,牺牲后的生长迟缓达到22%。两组的热量摄入相同,因此食物效率降低了40%。与体表面积相关的静息代谢增加了25%。体内去甲肾上腺素(NE)的生热作用(非寒颤产热试验)明显降低34%。BAT重量降低21%,但总蛋白和线粒体蛋白含量无变化。观察到每BAT嘌呤核苷酸结合增加26%(作为产热活性指标),表明所观察到的静息代谢增强主要是由于BAT产热活性增加。然而,BAT线粒体呼吸研究(更直接的功能测试)显示,棕榈酰肉碱或乙酰肉碱(均存在苹果酸)或α -甘油磷酸酯作为底物时,最大耗氧量明显降低约30%。这种最大BAT氧化能力受损可能解释了体内NE产热作用受损。还讨论了线粒体基底通透性可能增加的原因。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Non-shivering thermogenesis and brown adipose tissue activity in essential fatty acid deficient rats.

The effects of essential fatty acid (EFA) deficiency on energetic metabolism and interscapular brown adipose tissue (BAT) activity were examined in the cold acclimated rat. Weanling male Long-Evans rats were fed on a low fat semipurified diet (control diet, 2% sunflower oil; EFA deficient diet, 2% hydrogenated coconut oil) for 9 weeks. They were exposed at 5 degrees C for the last 5 weeks. In EFA deficient rats, compared to controls, growth retardation reached 22% at sacrifice. Caloric intake being the same in the two groups, it follows that food efficiency was decreased by 40%. Resting metabolism in relation to body surface area was 25% increased. Calorigenic effect of norepinephrine (NE) in vivo (test of non-shivering thermogenesis) underwent a marked decrease of 34%. BAT weight was 21% decreased but total and mitochondrial protein content showed no variation. A 26% increase in purine nucleotide binding per BAT (taken as an index of thermogenic activity) was observed, suggesting that the enhancement in resting metabolism observed was mainly due to increased BAT thermogenesis. However, BAT mitochondria respiratory studies which are more direct functional tests showed a marked impairment of maximal O2 consumption of about 30% with palmitoyl-carnitine or acetyl-carnitine (both in presence of malate) or with alpha-glycerophosphate as substrate. It is likely that this impaired maximal BAT oxidative capacity may explain the impaired NE calorigenic effect in vivo. A possible increase in mitochondrial basal permeability is also discussed.

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