Sherwin R, Wahren J, Felig P
Metabolism. 1976 Nov;25(11 Suppl 1):1381-3. doi: 10.1016/s0026-0495(76)80146-1.
Hypoglucagonemia (induced by somatostatin) and hyperglucagonemia (induced by infusion of physiologic amounts of glucagon) have only evanescent effects on blood glucose regulation. Despite on-going glucagon suppression by somatostatin, fasting hyperglycemia develops within 4-6 hr of insulin suppression, indicating that (1) basal glucagon secretion is not essential for the development of the diabetic state; and (2) insulin-deficiency (rather than altered glucagon secretion) is the dominant long-term factor determining glucose homeostasis in the diabetic. With respect to hyperglucagonemia, only a transient increase in splanchnic glucose output is observed in normal and diabetic subjects in response to physiologic increments in this hormone. The exaggerated hyperglycemic effect of glucagon observed in diabetics1 is thus a consequence of the failure to metabolize the glucose traniently released into the systemic circulation in response to the glucagon rather than a result of persistent stimulation of hepatic glucose production. These observations thus further underscore the essentiality of insulin deficiency in the diabetogenic action of glucagon.
低胰高血糖素血症（由生长抑素诱导）和高胰高血糖素血症（由输注生理量的胰高血糖素诱导）对血糖调节仅有短暂的影响。尽管生长抑素持续抑制胰高血糖素，但在胰岛素抑制后的4 - 6小时内仍会出现空腹高血糖，这表明：（1）基础胰高血糖素分泌对于糖尿病状态的发展并非必不可少；（2）胰岛素缺乏（而非胰高血糖素分泌改变）是决定糖尿病患者葡萄糖稳态的主要长期因素。关于高胰高血糖素血症，正常人和糖尿病患者在该激素生理性增加时，仅观察到内脏葡萄糖输出短暂增加。因此，糖尿病患者中观察到的胰高血糖素的过度高血糖作用是由于未能代谢因胰高血糖素而短暂释放到体循环中的葡萄糖，而非持续刺激肝脏葡萄糖生成的结果。这些观察结果进一步强调了胰岛素缺乏在胰高血糖素致糖尿病作用中的必要性。
