Goresky C A, Daly D S, Mishkin S, Arias I M
Am J Physiol. 1978 Jun;234(6):E542-53. doi: 10.1152/ajpendo.1978.234.6.E542.
The multiple-indicator dilution technique was utilized to examine the hepatic uptake of albumin-bound labeled palmitate from the portal vein blood of the pentobarbital-anesthetized dog, in a fasted state and after infusion of a variety of compounds that were expected to bind to Z protein, the cellular cytosolic protein binding free fatty acids, and their acyl-CoA derivatives. Analysis of the data indicates that after infusion of alpha-bromopalmitate, 16-bromo-9-hexadecenoate, and sulfobromophthalein sodium (which also bind to albumin), the palmitate label influx, efflux, and metabolic sequestration (removal of label from the pool of free fatty acids able to leave the cell) all increase and that, after infusion of flavaspidic acid, label efflux and metabolic sequestration increase. In vitro competitive binding studies carried out on the cellular cytosol indicat that the basis for the increase in efflux and metabolic sequestration is displacement of labeled palmitate from high affinity sites on the intracellular Z protein (which are presumably in equilibrium with and may be taken to be representative of other intracellular binding sites). These studies also suggest that increased uptake is due to similar displacement from high affinity sites on serum albumin.
采用多指标稀释技术，在禁食状态下以及输注各种预期会与Z蛋白（一种结合游离脂肪酸及其酰基辅酶A衍生物的细胞溶质蛋白）结合的化合物后，检测戊巴比妥麻醉犬门静脉血中白蛋白结合的标记棕榈酸酯的肝摄取情况。数据分析表明，输注α-溴棕榈酸酯、16-溴-9-十六碳烯酸酯和磺溴酞钠（它们也与白蛋白结合）后，棕榈酸酯标记物的流入、流出和代谢滞留（从能够离开细胞的游离脂肪酸池中去除标记物）均增加，而输注黄绵马酸后，标记物流出和代谢滞留增加。对细胞溶质进行的体外竞争性结合研究表明，流出和代谢滞留增加的基础是标记棕榈酸酯从细胞内Z蛋白上的高亲和力位点被置换（这些位点可能与其他细胞内结合位点处于平衡状态，可被视为其代表）。这些研究还表明，摄取增加是由于血清白蛋白上高亲和力位点的类似置换所致。
