Muñíz R, Burguillo L, del Castillo J R
Laboratorio de Fisiología Gastrointestinal, Instituto Venezolano de Investigaciones Científicas (IVIC), Caracas.
Pflugers Arch. 1993 Apr;423(1-2):59-66. doi: 10.1007/BF00374961.
The effects of starvation on neutral amino acid transport were examined in isolated enterocytes. Starvation stimulated L-alanine transport by the Na(+)-dependent system A and the Na(+)-independent system L without producing any changes in either the Na(+)-dependent systems ASC or the passive non-mediated uptake. Starvation produces a twofold increase in Vmax of system A without any change in Kt. Starvation produces an increase in Vmax of system L of 1.7 times without any change in Kt. Activation of systems A and L by starvation was reversible with subsequent refeeding. The effects of a series of amino acids on systems A and L were evaluated. A different inhibition pattern was found in starved animals as compared to controls. Starvation increases Na(+)-dependent L-alanine uptake and Na(+)-independent cycloleucine uptake by small-intestinal brush-border membrane vesicles. These results suggest that starvation stimulates amino acid transport across the apical plasma membrane of the enterocytes by inducing specific carrier units.
在分离的肠细胞中研究了饥饿对中性氨基酸转运的影响。饥饿通过钠依赖性A系统和钠非依赖性L系统刺激L-丙氨酸转运，而钠依赖性ASC系统或被动非介导摄取均未发生任何变化。饥饿使A系统的Vmax增加两倍，而Kt无任何变化。饥饿使L系统的Vmax增加1.7倍，而Kt无任何变化。饥饿对A系统和L系统的激活作用在随后重新喂食后是可逆的。评估了一系列氨基酸对A系统和L系统的影响。与对照相比，在饥饿动物中发现了不同的抑制模式。饥饿增加了小肠刷状缘膜囊泡对钠依赖性L-丙氨酸的摄取和钠非依赖性环亮氨酸的摄取。这些结果表明，饥饿通过诱导特定的载体单位刺激氨基酸跨肠细胞顶端质膜的转运。
