Brady P S, Marine K A, Brady L J, Ramsay R R
Food Science and Nutrition, University of Minnesota, St. Paul 55108.
Biochem J. 1989 May 15;260(1):93-100. doi: 10.1042/bj2600093.
The present studies examined the effect of agents that induce peroxisomal and mitochondrial beta-oxidation on hepatic mitochondrial carnitine palmitoyltransferase (CPT) and peroxisomal carnitine acyltransferase [CPTs of Ramsay (1988) Biochem. J. 249, 239-245; COT of Farrell & Bieber (1983) Arch. Biochem. Biophys. 222, 123-132 and Miyazawa, Ozasa, Osumi & Hashimoto (1983) J. Biochem. 94, 529-542]. In the first studies, high fat diets containing corn oil or fish oil were used to induce peroxisomal and mitochondrial enzymes. Rats were fed one of three diets for 4 weeks: (1) low fat, with corn oil as 11% of energy (kJ); (2) high fat, with corn oil as 45% of kJ; (3) high fat, with fish oil as 45% of kJ. At the end of 4 weeks, both mitochondrial CPT and peroxisomal CPTs exhibited increases in activity, immunoreactive protein, mRNA levels and transcription rates in livers of rats fed either high-fat diet compared to the low fat diet. Riboflavin deficiency or starvation for 48 h also increased the peroxisomal CPTs mRNA. A second set of studies used the plasticizer 2-(diethylhexyl)phthalate (DEHP), 0.5% clofibrate or 1% acetylsalicylic acid (fed for 3 weeks) to alter peroxisomal and mitochondrial fatty acid oxidation. With DEHP, the mitochondrial CPT and peroxisomal CPTs activity, immunoreactive protein, mRNA levels and and transcription rate were all increased by 3-5-fold. The peroxisomal CPTs activity, immunoreactive protein, mRNA levels and transcription rate were increased 2-3-fold by clofibrate and acetylsalicylic acid, again similar to mitochondrial CPT. The results of the combined studies using both diet and drugs to cause enzyme induction suggest that the synthesis of the carnitine acyltransferases (mitochondrial CPT and peroxisomal CPTs) may be co-ordinated with each other; however, the co-ordinate regulatory factors have not yet been identified.
本研究考察了诱导过氧化物酶体和线粒体β-氧化的试剂对肝脏线粒体肉碱棕榈酰转移酶(CPT)和过氧化物酶体肉碱酰基转移酶的影响[拉姆齐(1988年)《生物化学杂志》第249卷,第239 - 245页中的CPT;法雷尔和比伯(1983年)《生物化学与生物物理学报》第222卷,第123 - 132页以及宫泽、小笹、大见和桥本(1983年)《生物化学杂志》第94卷,第529 - 542页中的COT]。在第一项研究中,使用含玉米油或鱼油的高脂肪饮食来诱导过氧化物酶体和线粒体酶。大鼠被喂食三种饮食中的一种,持续4周:(1)低脂饮食,玉米油占能量(千焦)的11%;(2)高脂肪饮食,玉米油占千焦的45%;(3)高脂肪饮食,鱼油占千焦的45%。在4周结束时,与低脂饮食组相比,喂食任何一种高脂肪饮食的大鼠肝脏中的线粒体CPT和过氧化物酶体CPT在活性、免疫反应性蛋白、mRNA水平和转录速率方面均呈现增加。核黄素缺乏或饥饿48小时也会增加过氧化物酶体CPT的mRNA。第二项研究使用增塑剂邻苯二甲酸二(2 - 乙基己基)酯(DEHP)、0.5%的氯贝丁酯或1%的乙酰水杨酸(喂食3周)来改变过氧化物酶体和线粒体脂肪酸氧化。使用DEHP时,线粒体CPT和过氧化物酶体CPT的活性、免疫反应性蛋白、mRNA水平和转录速率均增加了3 - 5倍。氯贝丁酯和乙酰水杨酸使过氧化物酶体CPT的活性、免疫反应性蛋白、mRNA水平和转录速率增加了2 - 3倍,同样类似于线粒体CPT。使用饮食和药物联合诱导酶的综合研究结果表明,肉碱酰基转移酶(线粒体CPT和过氧化物酶体CPT)的合成可能相互协调;然而,尚未确定协调调节因子。