Ebert R, Creutzfeldt W, Brown J C, Frerichs H, Arnold R
Diabetologia. 1976 Dec;12(6):609-12. doi: 10.1007/BF01220638.
Twenty-nine patients with chronic pancreatitis had a significantly greater IR-GIP response to a test meal than 15 controls. This increased response was not related to the degree of steatorrhoea or glucose intolerance. It was most marked in a group of patients with moderately impaired IRI release and medium steatorrhoea. From this is concluded that the IR-GIP response to a test meal is determined by at least two factors: 1. feedback control via insulin secretion, 2. assimilation of fat. In chronic pancreatitis endocrine insufficiency may induce an exaggerated GIP response and severe exocrine insufficiency may prevent fat induced GIP release. Gastrin is not involved in the different GIP response in patients with chronic pancreatitis.
29例慢性胰腺炎患者对试餐的胰岛素释放依赖性胃抑肽（IR-GIP）反应显著高于15例对照组。这种增强的反应与脂肪泻程度或葡萄糖不耐受无关。在一组胰岛素释放中度受损和中度脂肪泻的患者中最为明显。由此得出结论，对试餐的IR-GIP反应至少由两个因素决定：1. 通过胰岛素分泌的反馈控制，2. 脂肪的吸收。在慢性胰腺炎中，内分泌功能不全可能导致胃抑肽反应过度，而严重的外分泌功能不全可能会阻止脂肪诱导的胃抑肽释放。胃泌素与慢性胰腺炎患者不同的胃抑肽反应无关。
