Hormonal regulation of glutamine metabolism by OK cells.
Hormonal regulation of glutamine metabolism by OK cells.
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OK 细胞对谷氨酰胺代谢的激素调节。
DOI：
10.1038/ki.1995.11
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发表时间：
1995
影响因子：
19.6
通讯作者：
Yudkoff,M
中科院分区：
文献类型：
--
作者：
Nissim,I;States,B;Nissim,I;Lin,ZP;Yudkoff,M
OK细胞对谷氨酰胺代谢的激素调节。甲状旁腺素、胰岛素或胰高血糖素调节肾脏谷氨酰胺和氨代谢的确切机制(S)尚不清楚。我们的目的是描述这些激素对肾脏谷氨酰胺代谢的影响和作用部位(S)。以OK细胞为模型系统进行了实验研究。细胞培养在pH 7.4的碳酸氢盐缓冲液中孵育3小时，其中添加1 mM[2-15N]或[5-15N]谷氨酰胺和10-7MPTH、胰岛素或胰高血糖素。在不含激素的pH值为6.8、7.4或7.6的条件下进行对比研究。甲状旁腺素和急性酸中毒通过磷酸依赖谷氨酰胺酶(PDG)和谷氨酸脱氢酶(GLDH)途径显著刺激谷氨酰胺代谢。而在pH值为7.6时则相反。胰岛素通过PDG增加血流量，但对GLDH途径影响不大。胰高血糖素对PDG或GLDH通路的影响均不显著。由[2-15N]谷氨酰胺形成的胞内[15N]谷氨酸部分通过转氨基转移为丙氨酸、天冬氨酸和丝氨酸，部分通过转位到胞外隔室。酸中毒、甲状旁腺素和胰岛素促进了[15N]丙氨酸的生成，而对[15N]天冬氨酸的影响不大。甲状旁腺素、胰岛素和胰高血糖素显著刺激[15N]丝氨酸的产生，而酸中毒作用不明显。酸中毒、甲状旁腺素和胰岛素引起细胞内谷氨酸转运显著增加，急性碱中毒引起细胞内谷氨酸转运减少。结果表明：(A)甲状旁腺素模拟急性酸中毒对肾脏谷氨酰胺代谢的影响，即通过PDG和GLDH途径促进谷氨酰胺代谢，并刺激细胞内谷氨酸的产生。这种作用可能是通过与细胞酸化相关的Na+-H+交换活性降低和/或通过第二信使介导的：(B)胰岛素，而不是胰升糖素，增加谷氨酰胺的摄取和代谢，同时增加细胞内谷氨酸的输出，足以刺激PDG途径；以及(C)总体上，与甲状旁腺素或胰岛素相比，胰高血糖素对OK细胞的谷氨酰胺代谢的影响很小。
Hormonal regulation of glutamine metabolism by OK cells. The precise mechanism(s) of action of PTH, insulin or glucagon in the regulation of renal glutamine and ammonia metabolism is unknown. Our aim was to delineate the effects and the site(s) of action of these hormones on renal glutamine metabolism. Experiments were carried out using OK cells as a model system. Cell cultures were incubated for three hours in a bicarbonate buffer of pH 7.4 supplemented with either 1 mM[2-15N] or [5-15N] glutamine and 10-7MPTH, insulin or glucagon. Comparative studies were performed at pH 6.8, 7.4 or 7.6 without hormone. PTH and acute acidosis significantly stimulated glutamine metabolism via both the phosphate-dependent glutaminase (PDG) and glutamate dehydrogenase (GLDH) pathways. The opposite was observed at pH 7.6. Insulin augmented flux via PDG with little effect on the GLDH pathway. Glucagon had insignificant effects on either PDG or GLDH pathways. Intracellular [15N] glutamate formed from [2-15N] glutamine was removed partially by transamination to alanine, aspartate and serine and partially by translocation to an extracellular compartment. Acidosis, PTH and insulin enhanced the formation of [15N] alanine with little effect on [15N] aspartate. PTH, insulin and glucagon significantly stimulated the production of [15N]serine, whereas acidosis had little effect. The translocation of intracellular glutamate was significantly increased by acidosis, PTH and insulin and decreased by acute alkalosis. The data indicate that: (a) PTH mimicks the effect of acute acidosis on renal glutamine metabolism, that is, augmented glutamine metabolism through both PDG and GLDH pathways and stimulated the output of intracellular glutamate. This effect might be mediated via decreased activity of the Na+-H+exchanger associated with cellular acidification and/or through a second messenger; (b) insulin, but not glucagon, increased glutamine uptake and metabolism, and simultaneously enhanced output of intracellular glutamate sufficiently to stimulate the PDG pathway; and (c) overall, glucagon had little effect on glutamine metabolism by OK cells compared with either PTH or insulin.
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DOI：
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