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首页> 外文期刊>The biochemical journal >Control of gluconeogenesis and of enzymes of glycogen metabolism in isolated rat hepatocytes. A parallel study of the effect of phenylephrine and of glucagon
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Control of gluconeogenesis and of enzymes of glycogen metabolism in isolated rat hepatocytes. A parallel study of the effect of phenylephrine and of glucagon

机译:分离的大鼠肝细胞中糖异生和糖原代谢酶的控制。苯肾上腺素和胰高血糖素作用的平行研究

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pHepatocytes isolated from the livers of fed rats were used for a comparative study of the effects of phenylephrine, vasopressin and glucagon on gluconeogenesis and on enzymes of glycogen metabolism. When hepatocytes were incubated in the presence of Casup2+/sup, phenylephrine stimulated gluconeogenesis from pyruvate less than did glucagon, but, in contrast with this hormone, it did not affect the activities of protein kinase and pyruvate kinase, nor the concentration of phosphoenolpyruvate, and it did not decrease the release of sup3/supHsub2/subO from [6-sup3/supH]glucose. The effects of vasopressin were similar to those of phenylephrine. Gluconeogenesis from fructose was also stimulated by phenylephrine and, more markedly, by glucagon at the expense of the conversion of fructose into lactate. Insulin was able to antagonize the stimulatory effect of phenylephrine on gluconeogenesis from pyruvate. When Casup2+/sup was removed from the incubation medium, phenylephrine still stimulated gluconeogenesis from pyruvate, but it also caused an activation of protein kinase and an inactivation of pyruvate kinase; accordingly, the concentration of phosphoenolpyruvate was increased, and, in contrast, vasopressin had no effect on all these parameters. The property of phenylephrine to cause the activation of glycogen phosphorylase was decreased by glucose or by the absence of Casup2+/sup; it was abolished when these two conditions were combined. Glycogen synthase was inactivated by phenylephrine in the presence or the absence of Casup2+/sup, although presumably by different mechanisms./p
机译:取自喂养大鼠肝脏的肝细胞用于比较研究去氧肾上腺素,加压素和胰高血糖素对糖异生和糖原代谢酶的影响。在存在Ca 2 + 的条件下孵育肝细胞时,去氧肾上腺素对丙酮酸的糖异生作用比胰高血糖素要少,但是与这种激素相反,它并不影响蛋白激酶和丙酮酸激酶的活性,磷酸烯醇丙酮酸的浓度,也没有降低<6-sup> 3 H]葡萄糖中 3 H 2 O的释放。加压素的作用与去氧肾上腺素相似。苯肾上腺素,更显着地,是胰高血糖素,也刺激了果糖产生的葡萄糖生成,其代价是果糖转化为乳酸。胰岛素能够拮抗去氧肾上腺素对丙酮酸中糖异生的刺激作用。当从培养液中除去Ca 2 + 时,去氧肾上腺素仍然刺激丙酮酸中的糖异生,但也引起蛋白激酶的活化和丙酮酸激酶的失活。因此,磷酸烯醇丙酮酸的浓度增加了,相反,加压素对所有这些参数没有影响。葡萄糖或缺少Ca 2 + 会降低去氧肾上腺素引起糖原磷酸化酶活化的特性;当这两个条件结合在一起时,它被废除了。在存在或不存在Ca 2 + 的情况下,去氧肾上腺素都能使糖原合酶失活,尽管推测可能是通过不同的机制造成的。

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