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胰抑制素33 - 49 C末端片段在大鼠体内的糖原分解和升血糖作用。

Glucogenolytic and hyperglycemic effect of 33-49 C-terminal fragment of pancreastatin in the rat in vivo.

作者信息

Sánchez-Margalet V, Calvo J R, Goberna R

机构信息

Departamento de Bioquímica Médica y Biología Molecular, Facultad de Medicina, Universidad de Sevilla, Spain.

出版信息

Horm Metab Res. 1992 Oct;24(10):455-7. doi: 10.1055/s-2007-1003361.

DOI:10.1055/s-2007-1003361
PMID:1464408
Abstract

The effects of the 33-49 C-terminal fragment of pancreastatin on glycogen content, glycemia, insulinemia and glucagonemia were studied in the rat in vivo. It was found that after intramesenteric vein injection of the peptide, the glycogen content of liver decreased compared with control group injected with saline-1 < % BSA. Blood glucose levels were increased by the C-terminal fragment of pancreastatin. This study shows that the 33-49 C-terminal fragment of pancreatasin could play a role in glucose metabolism not mediated by insulin or glucagon.

摘要

在大鼠体内研究了胰抑制素33 - 49 C末端片段对糖原含量、血糖、胰岛素血症和胰高血糖素血症的影响。结果发现,经肠系膜静脉注射该肽后,与注射含1%牛血清白蛋白的生理盐水的对照组相比,肝脏糖原含量降低。胰抑制素C末端片段使血糖水平升高。本研究表明,胰抑制素33 - 49 C末端片段可能在不通过胰岛素或胰高血糖素介导的葡萄糖代谢中发挥作用。

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Glucogenolytic and hyperglycemic effect of 33-49 C-terminal fragment of pancreastatin in the rat in vivo.胰抑制素33 - 49 C末端片段在大鼠体内的糖原分解和升血糖作用。
Horm Metab Res. 1992 Oct;24(10):455-7. doi: 10.1055/s-2007-1003361.
2
Pancreastatin and its 33-49 C-terminal fragment inhibit glucagon-stimulated insulin in vivo.胰抑制素及其33 - 49 C末端片段在体内可抑制胰高血糖素刺激的胰岛素分泌。
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Glycogenolytic effect of pancreastatin in the rat.胰抑制素对大鼠的糖原分解作用。
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Bioactivity of synthetic C-terminal fragment of rat pancreastatin on endocrine pancreas.大鼠胰抑制素合成C末端片段对内分泌胰腺的生物活性
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Pancreastatin (33-49) enhances the priming effect of glucose in the rat pancreas.胰抑制素(33 - 49)增强了葡萄糖对大鼠胰腺的启动作用。
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