Raskin P, Unger R H
Med Clin North Am. 1978 Jul;62(4):713-22. doi: 10.1016/s0025-7125(16)31767-9.
We have considered the evidence, first, that the presence of glucagon is essential in the pathogenesis of the full syndrome that results from complete insulin deficiency; second, that in the diabetic in whom insulin levels are relatively fixed, a rise in glucagon concentration contributes to endogenous hyperglycemia; and, third, that conventional methods of treatment of diabetes do not fully correct either the abnormal glucagon levels or the hyperglycemia, but when insulin therapy is supplemented with somatostatin, an agent which suppresses both glucagon and growth hormone, both hyperglycemia and hyperglucagonemia are corrected. These facts may one day provide a rationale for therapeutic efforts to suppress excess glucagon secretion in the management of diabetes in man.
其一，胰高血糖素的存在对于完全胰岛素缺乏所致的完整综合征的发病机制至关重要；其二，在胰岛素水平相对固定的糖尿病患者中，胰高血糖素浓度的升高会导致内源性高血糖；其三，传统的糖尿病治疗方法并不能完全纠正异常的胰高血糖素水平或高血糖，但当胰岛素治疗辅以生长抑素（一种可抑制胰高血糖素和生长激素的药物）时，高血糖和高胰高血糖素血症均可得到纠正。这些事实或许有朝一日能为在人类糖尿病管理中抑制过量胰高血糖素分泌的治疗努力提供理论依据。
