Uptake and metabolism of fatty acids by dispersed adult rat heart myocytes. I. Kinetics of homologous fatty acids.
Uptake and metabolism of fatty acids by dispersed adult rat heart myocytes. I. Kinetics of homologous fatty acids.
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DOI：
10.1016/s0021-9258(18)43454-0
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发表时间：
1980-10
期刊：
影响因子：
--
通讯作者：
R. DeGrella;R. Light
中科院分区：
文献类型：
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作者：
R. DeGrella;R. Light
成年大鼠心肌细胞制备用于研究在37 ℃下不存在血清白蛋白的情况下1-（14）C标记的游离脂肪酸癸酸酯、月桂酸酯、肉豆蔻酸酯、棕榈酸酯和油酸酯的摄取和代谢。总摄取率由不饱和组分和饱和组分组成。不饱和组分对应于在游离脂肪酸馏分中积累的脂肪酸，并且这种积累的速率随链长的函数呈抛物线增加。可饱和组分对应于转化为唯一可检测代谢产物的脂肪酸部分：CO2、甘油三酯和极性脂质。该过程的Km约为1 μ M，与链长无关。饱和组分的Vmax仅随链长轻微变化，从癸酸酯的20 +/- 1 nmol/h-mg细胞蛋白到棕榈酸酯的47 +/- 18 nmol/h-mg细胞蛋白。然而，相对产物分布确实随链长而变化，范围从癸酸酯的主要二氧化碳到棕榈酸酯的大约等量的二氧化碳、甘油三酯和极性脂质。两个内部池的游离脂肪酸被假定：一个小池，平衡迅速与外部脂肪酸，并作为脂肪酸活化的前体，和一个主要的池含有大部分积累的游离酸。这两个资源库是可以相互转换的。数据支持一个简单的扩散或膜分配过程中积累的脂肪酸在第二池。本文中提供的数据不足以区分简单扩散或载体介导的吸收到第一池中的过程。观察到的饱和动力学似乎代表了代谢步骤，如脂肪酸活化，而不是运输载体。较高浓度的长链脂肪酸的毒性证据限制了在不存在白蛋白的情况下可以研究的浓度范围。癸酸在浓度高达300 μ M时似乎没有毒性，但10 μ M的月桂酸和5 μ M的肉豆蔻酸似乎会解除呼吸控制。
An adult rat heart myocyte preparation was used to study the uptake and metabolism of the 1-(14)C-labeled free fatty acids decanoate, laurate, myristate, palmitate, and oleate at 37 degrees C in the absence of serum albumin. The rate of total uptake consisted of both a nonsaturable and a saturable component. The nonsaturable component corresponded to the fatty acid accumulating in the free fatty acid fraction, and the rate of this accumulation increased logarithmically as a function of chain length. The saturable component corresponded to that portion of fatty acid converted to the only detectable metabolic products: CO2, triglyceride, and polar lipid. The Km for this process was about 1 microM and was independent of chain length. The Vmax for the saturable component varied only slightly with chain length, from 20 +/- 1 nmol/h-mg of cell protein for decanoate to 47 +/- 18 nmol/h-mg of cell protein for palmitate. The relative product distribution did vary with chain length, however, ranging from primarily carbon dioxide for decanoate to approximately equal quantities of carbon dioxide, triglyceride, and polar lipid for palmitate. Two internal pools of free fatty acid are postulated: a minor pool that equilibrates rapidly with external fatty acid and serves as the precursor for fatty acid activation, and a major pool containing most of the accumulated free acid. These two pools are interconvertible. The data support a simple diffusion or membrane-partitioning process for the accumulation of fatty acid in the second pool. The data presented in this paper are not sufficient to distinguish between a simple diffusion or a carrier-mediated process for uptake into the first pool. The saturation kinetics observed appear to represent a metabolic step such as fatty acid activation, rather than a transport carrier. Evidence of toxicity at a higher concentration of the longer chain fatty acids limits the concentration range that can be studied in the absence of albumin. Decanoate did not appear to be toxic at concentrations up to 300 microM, but laurate at 10 microM and myristate at 5 microM appeared to uncouple respiratory control.