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首页> 外文期刊>Journal of Cellular Physiology >Role of amino acid-induced changes in ion fluxes in the regulation of hepatic protein synthesis.
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Role of amino acid-induced changes in ion fluxes in the regulation of hepatic protein synthesis.

机译：氨基酸的作用段离子通量的变化在调节肝脏蛋白质合成。

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摘要

Alanine is a powerful stimulator of hepatic protein synthesis whose mechanism of action has not yet been ascertained. The present work aimed to elucidate whether rate changes in ion fluxes accompanying the transport of this amino acid could play a role in the stimulation of protein synthesis. In perfused livers, the utilization of alanine produced a net uptake of K+ of 1.5 mumol/min/liver, a progressively increasing efflux of Ca2+ to reach a maximum of 0.9 mumol/min/liver, and alkalization of the extracellular medium. Inhibition of Na+/K+ exchange by ouabain reversed only the uptake of K+, indicating that this is the main way for the efflux of Na+ cotransported with alanine. In isolated hepatocytes, the uptake of alanine increased the intracellular content of K+ and the cell volume. The following observations suggest that these changes, and not an increased intracellular concentration of Na+, are associated with the stimulation of protein synthesis: 1) Ouabain inhibited the alanine stimulation of L-[3H]-valine incorporation into protein without altering the basal rate of protein labeling; 2) ouabain had no effects on alanine uptake indicating that Na+ influx is not involved in the alanine stimulation of protein synthesis; 3) disruption of Na+ gradient across the plasma membrane by specific ionophores, monensin and gramicidin D, inhibited both basal and alanine-stimulated protein synthesis, but substitution of extracellular Na+ by K+ did not prevent the stimulatory action of alanine. The observation that hypotonic buffer enhanced protein synthesis to the same degree than alanine in liver cells indicates that alanine-induced cell swelling could be sufficient to stimulate protein synthesis.
机译：肝的丙氨酸是一种强大的刺激蛋白质合成的作用机理尚未确定。阐明是否率离子通量的变化伴随这种氨基酸的运输可以扮演一个角色在蛋白质的刺激吗合成。丙氨酸产生的净吸收K + 1.5mumol /分钟/肝,逐步增加流出的Ca2 +最多达到0.9mumol /分钟/肝脏和碱性化的细胞外介质。通过只乌本苷逆转的交换K +,表示这是主要方式射流与丙氨酸Na +协同转运。孤立的肝细胞,丙氨酸的吸收增加了K +和细胞内的内容细胞体积。这些变化,而不是增加细胞内的浓度Na +与蛋白质的刺激有关综合:1)乌本苷抑制丙氨酸刺激L - [3 h]缬氨酸并入在不改变基底的蛋白质蛋白质标记;丙氨酸摄取表明Na +涌入参与的丙氨酸刺激蛋白质合成;质膜的特定的离子载体,莫能菌素和短杆菌肽D,抑制基底和alanine-stimulated蛋白质合成,但是替换的细胞外Na + K +没有防止丙氨酸的刺激作用。加强观察,低渗的缓冲区比丙氨酸蛋白质合成到相同的程度在肝细胞表明alanine-induced细胞肿胀可能足以刺激蛋白质合成。

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