Ohneda A, Kobayashi T, Nihei J, Nishikawa K
Horm Metab Res. 1981 Apr;13(4):207-11. doi: 10.1055/s-2007-1019222.
In order to investigate the relationship between the development of diabetes mellitus and glucagon, experimental studies were performed in genetically diabetic mice (KKA gamma and KK B1) and in C57 mice of various ages. In the KK mice, the fasting plasma glucose increased during the aging process and reached the maximum at 14 weeks. The fasting plasma insulin in the KK mice was significantly elevated during the aging process and continued to increase till 20 weeks of age. In contrast, an increase in the fasting plasma glucagon was observed only at the age of 4 weeks, although the plasma glucagon increased during the aging process. The content of the insulin in the pancreas of the KK mice was significantly higher than that of the C57 mice, continuing to increase during the aging process. the glucagon content of the pancreas increased during the aging process but no significant difference was observed between the KK mice and the control mice. The total immunoreactive glucagon in the jejunum measured by non-specific antiserum was slightly reduced in the KK mice at the age of 14 weeks, compared with the C57 mice. There was no difference in the glucagon content of the stomach between the KK mice and the C57 mice of various ages. The KK mice at 14 weeks showed an elevated plasma glucagon 30 min after glucose injection, compared with the C57 mice, which indicates a reduced suppression of glucagon in response to hyperglycemia in the KK mice. The plasma glucagon in the KK mice 30 min after arginine was slightly higher than in the control mice, although not significantly so. From these results it was concluded that the KK mice revealed an elevation of fasting plasma glucagon in the early stage of diabetes mellitus and a decrease in glucose-induced glucagon suppression at 14 weeks and that diabetes mellitus in the KK mice derived mainly from insulin resistance associated with hyperinsulinemia.
为了研究糖尿病的发展与胰高血糖素之间的关系，我们对遗传性糖尿病小鼠（KKAγ和KK B1）以及不同年龄段的C57小鼠进行了实验研究。在KK小鼠中，空腹血糖在衰老过程中升高，并在14周时达到最大值。KK小鼠的空腹血浆胰岛素在衰老过程中显著升高，并持续增加直至20周龄。相比之下，尽管血浆胰高血糖素在衰老过程中有所增加，但仅在4周龄时观察到空腹血浆胰高血糖素的增加。KK小鼠胰腺中的胰岛素含量显著高于C57小鼠，并在衰老过程中持续增加。胰腺中的胰高血糖素含量在衰老过程中增加，但KK小鼠与对照小鼠之间未观察到显著差异。与C57小鼠相比，14周龄的KK小鼠用非特异性抗血清测得的空肠中总免疫反应性胰高血糖素略有降低。不同年龄段的KK小鼠和C57小鼠胃中的胰高血糖素含量没有差异。与C57小鼠相比，14周龄的KK小鼠在注射葡萄糖后30分钟血浆胰高血糖素升高，这表明KK小鼠对高血糖症引起的胰高血糖素抑制作用减弱。精氨酸注射后30分钟，KK小鼠的血浆胰高血糖素略高于对照小鼠，尽管差异不显著。从这些结果可以得出结论，KK小鼠在糖尿病早期空腹血浆胰高血糖素升高，在14周时葡萄糖诱导的胰高血糖素抑制作用降低，并且KK小鼠的糖尿病主要源于与高胰岛素血症相关的胰岛素抵抗。
