Donowitz M, Hendler R, Spiro H M, Binder H J, Felig P
Ann Intern Med. 1975 Dec;83(6):778-81. doi: 10.7326/0003-4819-83-6-778.
Plasma pancreatic glucagon concentrations were determined in the basal state and after the infusion of alanine in 10 patients with acute pancreatitis (5 in an initial episode of pancreatitis), in 10 patients with chronic pancreatic insufficiency, and in 21 healthy controls. In acute pancreatitis, basal glucagon levels were nine times normal but were higher during the initial attack than with a history of previous attacks. The glucagon response to alanine was also increased threefold to fourfold in initial attacks. In contrast, after recovery from the initial attack of acute pancreatitis, during acute episodes of pancreatitis in patients with a history of previous attacks, and in patients with pancreatic insufficiency, alanine failed to elicit a consistent rise in plasma glucagon. The data suggest that hyperglucagonemia may contribute to the hyperglycemia of acute pancreatitis, particularly during the initial episode. Loss of alpha cell responsiveness to alanine provides a sensitive index of previous pancreatitis.
对10例急性胰腺炎患者（其中5例为首次发作胰腺炎）、10例慢性胰腺功能不全患者及21名健康对照者测定了基础状态下及输注丙氨酸后的血浆胰高血糖素浓度。在急性胰腺炎患者中，基础胰高血糖素水平为正常的9倍，但在首次发作时高于既往有发作史者。在首次发作时，胰高血糖素对丙氨酸的反应也增加了3至4倍。相比之下，在急性胰腺炎首次发作恢复后、既往有发作史的患者胰腺炎急性发作期间以及胰腺功能不全患者中，丙氨酸未能引起血浆胰高血糖素持续升高。数据表明，高胰高血糖素血症可能导致急性胰腺炎患者的高血糖，尤其是在首次发作期间。α细胞对丙氨酸反应性的丧失是既往胰腺炎的一个敏感指标。
