Sala-Rabanal Monica, Loo Donald D F, Hirayama Bruce A, Turk Eric, Wright Ernest M
Department of Physiology, David Geffen School of Medicine at UCLA, 10833 Le Conte Avenue, 53-330 CHS, Los Angeles, California 90095-1751, USA.
J Physiol. 2006 Jul 1;574(Pt 1):149-66. doi: 10.1113/jphysiol.2006.107904. Epub 2006 Apr 20.
The human intestinal proton-coupled oligopeptide transporter hPEPT1 has been implicated in the absorption of pharmacologically active compounds. We have investigated the interactions between a comprehensive selection of drugs, and wild-type and variant hPEPT1s expressed in Xenopus oocytes, using radiotracer uptake and electrophysiological methods. The beta-lactam antibiotics ampicillin, amoxicillin, cephalexin and cefadroxil, the antineoplastics delta-aminolevulinic acid (delta-ALA) and bestatin, and the neuropeptide N-acetyl-Asp-Glu (NAAG), were transported, as judged by their ability to evoke inward currents. When the drugs were added in the presence of the typical substrate glycylsarcosine (Gly-Sar), the inward currents were equal or less than that induced by Gly-Sar alone. This suggests that the drugs are transported at a lower turnover rate than Gly-Sar, but may also point towards complex interactions between dipeptides, drugs and the transporter. Gly-Sar and the drugs also modified the kinetics of hPEPT1 presteady-state charge movement, by causing a reduction in maximum charge (Qmax) and a shift of the midpoint voltage (V0.5) to more negative potentials. Our results indicate that the substrate selectivity of hPEPT1 is: Gly-Sar > NAAG, delta-ALA, bestatin > cefadroxil, cephalexin > ampicillin, amoxicillin. Based on steady-state and presteady-state analysis of Gly-Sar and cefadroxil transport, we proposed an extension of the 6-state kinetic model for hPEPT1 function that globally accounts for the observed presteady-state and steady-state kinetics of neutral dipeptide and drug transport. Our model suggests that, under saturating conditions, the rate-limiting step of the hPEPT1 transport cycle is the reorientation of the empty carrier within the membrane. Variations in rates of drug cotransport are predicted to be due to differences in affinity and turnover rate. Oral availability of drugs may be reduced in the presence of physiological concentrations of dietary dipeptides in the gut, suggesting that oral delivery drugs should be taken on an empty stomach. The common hPEPT1 single-nucleotide polymorphisms Ser117Asn and Gly419Ala retained the essential kinetic and drug recognition characteristics of the wild type, suggesting that neither variant is likely to have a major impact on oral absorption of drugs.
人类肠道质子偶联寡肽转运体hPEPT1与药理活性化合物的吸收有关。我们使用放射性示踪摄取和电生理方法,研究了一系列药物与非洲爪蟾卵母细胞中表达的野生型和变异型hPEPT1之间的相互作用。通过它们引发内向电流的能力判断,β-内酰胺抗生素氨苄西林、阿莫西林、头孢氨苄和头孢羟氨苄、抗肿瘤药δ-氨基乙酰丙酸(δ-ALA)和贝司他汀以及神经肽N-乙酰天冬氨酸-谷氨酸(NAAG)均可被转运。当在典型底物甘氨酰肌氨酸(Gly-Sar)存在的情况下加入这些药物时,内向电流等于或小于单独由Gly-Sar诱导的电流。这表明这些药物的转运周转率低于Gly-Sar,但也可能表明二肽、药物和转运体之间存在复杂的相互作用。Gly-Sar和这些药物还通过导致最大电荷量(Qmax)降低以及中点电压(V0.5)向更负电位偏移,改变了hPEPT1预稳态电荷移动的动力学。我们的结果表明,hPEPT1的底物选择性为:Gly-Sar > NAAG、δ-ALA、贝司他汀 > 头孢羟氨苄、头孢氨苄 > 氨苄西林、阿莫西林。基于对Gly-Sar和头孢羟氨苄转运的稳态和预稳态分析,我们提出了hPEPT1功能的六态动力学模型的扩展,该模型全面解释了观察到的中性二肽和药物转运的预稳态和稳态动力学。我们的模型表明,在饱和条件下,hPEPT1转运循环的限速步骤是空载体在膜内的重新定向。预计药物共转运速率的差异是由于亲和力和周转率的不同。肠道中存在生理浓度的膳食二肽时,药物的口服可用性可能会降低,这表明口服给药的药物应空腹服用。常见的hPEPT1单核苷酸多态性Ser117Asn和Gly419Ala保留了野生型的基本动力学和药物识别特征,这表明这两种变异体都不太可能对药物的口服吸收产生重大影响。