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链脲佐菌素和烟酰胺诱导的胰岛素分泌肿瘤发展过程中的胰高血糖素分泌。

Glucagon secretion during the development of insulin-secreting tumors induced by streptozotocin and nicotinamide.

作者信息

Yoshino G, Kazumi T, Morita S, Kobayashi N, Terashi K, Baba S

出版信息

Endocrinol Jpn. 1979 Dec;26(6):655-60. doi: 10.1507/endocrj1954.26.655.

Abstract

Serial oral glucose tolerance tests in rats treated with streptozotocin and nicotinamide showed that blood glucose levels after glucose loading were suppressed significantly 7 months after treatment as compared to those of earlier stages. Post-glucose plasma insulin levels were significantly elevated at the 9th to 12th month and concomitantly fasting plasma glucagon levels rose significantly. At that time pancreatic islet cell tumors were demonstrated in all of the rats in this experiment. Post-glucose plasma glucagon levels, however, did not show remarkable changes throughout the observation. In spite of hyperinsulinemia, post-glucose plasma glucagon levels of tumor-bearing rats were significantly lower than those of body weight adjusted controls. It is inferred from the study that secretory activity of pancreatic A-cells of tumor-bearing rats is restrained by excess insulin released from islet cell tumors.

摘要

对用链脲佐菌素和烟酰胺处理的大鼠进行连续口服葡萄糖耐量试验,结果显示,与早期阶段相比,治疗7个月后,葡萄糖负荷后的血糖水平显著降低。葡萄糖负荷后血浆胰岛素水平在第9至12个月显著升高,同时空腹血浆胰高血糖素水平也显著升高。当时,本实验所有大鼠均出现胰岛细胞瘤。然而,在整个观察过程中,葡萄糖负荷后血浆胰高血糖素水平未显示出明显变化。尽管存在高胰岛素血症,但荷瘤大鼠葡萄糖负荷后血浆胰高血糖素水平显著低于体重匹配的对照组。从该研究推断,荷瘤大鼠胰腺A细胞的分泌活性受到胰岛细胞瘤释放的过量胰岛素的抑制。

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