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肥胖 Zucker 大鼠肝脏中 Na⁺ 依赖性转运系统与 Na⁺,K⁺ -ATP 酶的协同诱导作用

Coordinate induction of Na(+)-dependent transport systems and Na+,K(+)-ATPase in the liver of obese Zucker rats.

作者信息

Ruiz-Montasell B, Ferrer-Martinez A, Casado F J, Felipe A, Pastor-Anglada M

机构信息

Departament de Bioquímica i Fisiologia, Universitat de Barcelona, Facultat de Biologia, Spain.

出版信息

Biochim Biophys Acta. 1994 Nov 23;1196(1):45-50. doi: 10.1016/0005-2736(94)90293-3.

DOI:10.1016/0005-2736(94)90293-3
PMID:7986809
Abstract

Solute uptake into liver plasma membrane vesicles from either lean or obese Zucker rats was monitored. D-Glucose and L-leucine uptakes at physiological concentrations of the substrate were not different in lean and obese Zucker rats. In agreement with a previous report (Ruiz et al. (1991) Biochem. J. 280, 367-372) L-alanine uptake was significantly enhanced in those preparations from obese animals. Na(+)-coupled uridine transport was markedly enhanced also in obese rats. The effect was due to an increase in Vmax (5.5 +/- 0.6 vs. 2.1 +/- 0.2 pmol/mg protein per 3 s, P < 0.01) without any significant change in Km (11.0 +/- 2.8 vs. 9.0 +/- 2.7 microM for obese and lean rats, respectively). Na+,K(+)-ATPase activity was also higher in liver plasma membrane vesicles from rat liver and it correlated with a higher amount of alpha 1-subunit protein in both, plasma membrane vesicles and homogenates from obese rat livers. In summary, in the hypertrophic liver of obese Zucker rats a coordinate induction of several Na(+)-dependent transport systems occurs and, in order to sustain the metabolic pressure associated with this adaptation, a significant induction of the Na+,K(+)-ATPase expression is also found. These data also provide new evidence for regulation of the recently characterized Na(+)-dependent nucleoside transporter.

摘要

监测了来自瘦型或肥胖型 Zucker 大鼠的肝质膜囊泡对溶质的摄取情况。在生理底物浓度下,瘦型和肥胖型 Zucker 大鼠对 D - 葡萄糖和 L - 亮氨酸的摄取没有差异。与之前的一份报告(Ruiz 等人,(1991) Biochem. J. 280, 367 - 372)一致,肥胖动物制备物中 L - 丙氨酸的摄取显著增强。肥胖大鼠中 Na⁺ 偶联的尿苷转运也明显增强。这种效应是由于 Vmax 的增加(每 3 秒 5.5 ± 0.6 对 2.1 ± 0.2 pmol/mg 蛋白,P < 0.01),而 Km 没有任何显著变化(肥胖大鼠和瘦型大鼠分别为 11.0 ± 2.8 对 9.0 ± 2.7 μM)。大鼠肝脏肝质膜囊泡中的 Na⁺,K⁺ - ATP 酶活性也更高,并且与肥胖大鼠肝脏的质膜囊泡和匀浆中 α1 - 亚基蛋白的含量更高相关。总之,在肥胖型 Zucker 大鼠的肥大肝脏中,几种 Na⁺ 依赖性转运系统发生协同诱导,并且为了维持与这种适应相关的代谢压力,还发现了 Na⁺,K⁺ - ATP 酶表达的显著诱导。这些数据也为最近鉴定的 Na⁺ 依赖性核苷转运体的调节提供了新证据。

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