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小鼠肝脏中糖原分解增强会刺激抗坏血酸的合成。

Ascorbic acid synthesis is stimulated by enhanced glycogenolysis in murine liver.

作者信息

Braun L, Garzó T, Mandl J, Bánhegyi G

机构信息

1st Institute of Biochemistry, Semmelweis Medical University, Budapest, Hungary.

出版信息

FEBS Lett. 1994 Sep 19;352(1):4-6. doi: 10.1016/0014-5793(94)00905-8.

Abstract

Ascorbic acid synthesis was stimulated by glucagon, dibutyryl cyclic AMP, as well as phenylephrine vasopressin or okadaic acid, in hepatocytes prepared from fed mice. However, no such effect was observed in glycogen-depleted cells from starved animals, either in the presence or absence of glucose. The rate of ascorbate synthesis showed close correlation with the glucose release by hepatocytes. In mice the injection of glucagon increased plasma ascorbate concentration fifteenfold, and caused a sixfold elevation of the ascorbate content of the liver. These results show that hepatic ascorbate synthesis is dependent on glycogenolysis, and indicate a regulatory role of ascorbate released by the liver.

摘要

在由喂食小鼠制备的肝细胞中,抗坏血酸的合成受到胰高血糖素、二丁酰环磷酸腺苷、去氧肾上腺素、血管加压素或冈田酸的刺激。然而,在饥饿动物的糖原耗尽细胞中,无论有无葡萄糖,均未观察到这种效应。抗坏血酸合成速率与肝细胞释放葡萄糖的速率密切相关。在小鼠中,注射胰高血糖素可使血浆抗坏血酸浓度增加15倍,并使肝脏中抗坏血酸含量提高6倍。这些结果表明,肝脏抗坏血酸的合成依赖于糖原分解,并提示肝脏释放的抗坏血酸具有调节作用。

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