Weisiger R A, Fitz J G, Scharschmidt B F
Department of Medicine, University of California, San Francisco 94143.
J Clin Invest. 1989 Feb;83(2):411-20. doi: 10.1172/JCI113899.
Recent observations suggest that the hepatic uptake of oleate may be sodium coupled. To assess the electrochemical forces driving fatty acid uptake, we used microelectrodes to monitor continuously the electrical potential difference across the plasma membrane in the perfused rat liver while simultaneously monitoring the rate of tracer [3H]oleate uptake from 1% albumin solutions. Isosmotic cation or anion substitution was used to vary the potential difference over the physiologic range. Depolarization of cells from -29 to -19 mV by substituting gluconate for chloride reduced steady-state oleate uptake by 34%. Conversely, hyperpolarization of cells to -52 mV by substituting nitrate for chloride increased uptake by 41%. Replacement of perfusate sodium with choline depolarized the cells to -18 mV and reduced uptake by 58%, an amount greater than expected from the degree of depolarization alone. Oleate in higher concentrations (1.5 mM in 2% albumin) depolarized cells by 3 mV in the presence of sodium, but had no effect in sodium-free buffer. These results suggest that a portion of oleate uptake in the intact liver occurs by electrogenic sodium cotransport. Uptake appears to be driven by both the electrical and sodium chemical gradients across the plasma membrane.
最近的观察结果表明，油酸的肝脏摄取可能与钠偶联。为了评估驱动脂肪酸摄取的电化学驱动力，我们使用微电极连续监测灌注大鼠肝脏中质膜两侧的电位差，同时监测示踪剂[3H]油酸从1%白蛋白溶液中的摄取速率。采用等渗阳离子或阴离子替代在生理范围内改变电位差。用葡萄糖酸盐替代氯化物使细胞从-29 mV去极化至-19 mV，使稳态油酸摄取减少34%。相反，用硝酸盐替代氯化物使细胞超极化至-52 mV，摄取增加41%。用胆碱替代灌注液中的钠使细胞去极化至-18 mV，摄取减少58%，减少量大于仅由去极化程度预期的量。在有钠存在的情况下，较高浓度（2%白蛋白中1.5 mM）的油酸使细胞去极化3 mV，但在无钠缓冲液中无作用。这些结果表明，完整肝脏中一部分油酸摄取是通过电致钠共转运发生的。摄取似乎由跨质膜的电和钠化学梯度驱动。
