Luyckx A
Diabete Metab. 1975 Sep;1(3):201-8.
Glucagon is secreted not only by A2-cells of the pancreatic islets but also by A cells in the gastric fundus and duodenum. Several reports have demonstrated that the glucagon plasma concentration is increased in genetic diabetes as well as in many conditions associated with a decreased glucose tolerance such as hepatic cirrhosis, myocardial infarction, infectious diseases, burns, taumatic shock, glucagonomas, acute pancreatitis, acromegaly, pheochromacytoma and Cushing's syndrome. Hyperglucagonemia is particularly important in diabetic ketoacidosis and in non-ketotic hyperosmolar coma. The mechanisms responsible for the diabetic's hyperglucagonemia remain controversial. According to several authors, the increased glucagon secretion is, for its main part, secondary to a prolonged defect in insulin secretion and thus relatively insensitive to an acute insulin administration. According to others, the A cell abnormality is of primary origin, independant from insulin deficiency and its effects are cumulative with those of the insulin lack. Several reports dealing with induced or spontaneous experimental diabetes are in favor of the first or the second hypothesis. It appears likely that glucagon plays a role in the metabolic derangments of diabetes. Indeed, hepatic glucose production is closely related to the ratio of molar concentrations of insulin and glucagon. Finally, in insulin-dependant diabetics, somatostatin infusion reduces plasma glucagon concentration and blood glucose and prevents the development of ketosis after withdrawal of insulin therapy. These results illustrate the contribution of glucagon in the pathogenesis of hyperglycemia and ketosis. Several arguments have been accumulated in favor of the following concept: diabetes hyperglycemia results both from glucose under-utilization secondary to insulin lack and from hepatic glucose over-production due to glucagon excess. Although controversial, the role of glucagon in ketogenesis appears likely.
胰高血糖素不仅由胰岛的A2细胞分泌，胃底和十二指肠的A细胞也可分泌。多项报告表明，在遗传性糖尿病以及许多糖耐量降低的情况下，如肝硬化、心肌梗死、传染病、烧伤、创伤性休克、胰高血糖素瘤、急性胰腺炎、肢端肥大症、嗜铬细胞瘤和库欣综合征，血浆胰高血糖素浓度会升高。高胰高血糖素血症在糖尿病酮症酸中毒和非酮症高渗性昏迷中尤为重要。糖尿病患者高胰高血糖素血症的发病机制仍存在争议。一些作者认为，胰高血糖素分泌增加主要是由于胰岛素分泌长期缺陷继发所致，因此对急性胰岛素给药相对不敏感。另一些人则认为，A细胞异常是原发性的，独立于胰岛素缺乏，其作用与胰岛素缺乏的作用累加。几项关于诱导性或自发性实验性糖尿病的报告支持第一种或第二种假设。胰高血糖素似乎在糖尿病的代谢紊乱中起作用。事实上，肝脏葡萄糖生成与胰岛素和胰高血糖素的摩尔浓度比密切相关。最后，在胰岛素依赖型糖尿病患者中，输注生长抑素可降低血浆胰高血糖素浓度和血糖，并在停止胰岛素治疗后防止酮症的发生。这些结果说明了胰高血糖素在高血糖和酮症发病机制中的作用。已有多项论据支持以下观点：糖尿病高血糖既源于胰岛素缺乏导致的葡萄糖利用不足，也源于胰高血糖素过量导致的肝脏葡萄糖生成过多。尽管存在争议，但胰高血糖素在酮体生成中的作用似乎是可能的。
