Creutzfeldt W, Ebert R, Nauck M, Stöckmann F
Scand J Gastroenterol Suppl. 1983;82:111-9.
The entero-insular axis comprises direct substrate stimulation of the islet cells by the absorbed nutrients and signal transmission by endocrine factors and nerves. The extent of neural influences has not yet been evaluated. GIP is the main incretin candidate. GIP release is dependent on nutrient absorption. Therefore, GIP abnormalities occur in a large number of gastrointestinal and metabolic diseases. These secondary changes are rarely of clinical significance. GIP hypersecretion may, however, contribute to the increased lipogenesis in obesity and the hypoglycemia in the late dumping syndrome. In type II diabetes hyper- and hyposecretion of GIP has been found but no correlation between GIP and insulin response. GIP abnormalities are not identical with disturbances of the entero-insular axis. These can only be evaluated by estimating the incretin effect (comparing the insulin response to oral glucose with the insulin response to an isoglycaemic iv glucose infusion). A decreased incretin effect has been observed in patients with jejuno-ileal bypass and in type II diabetes. In neither condition was a correlation found between incretin effect and GIP response. It is concluded that disturbances of the entero-insular axis are rarely explained by GIP abnormalities. Therefore, other humoral gut factors must exist. Also the neural part of the entero-insular axis requires exploration in health and disease.
肠-胰岛轴包括吸收的营养物质对胰岛细胞的直接底物刺激以及内分泌因子和神经的信号传递。神经影响的程度尚未得到评估。胃抑肽是主要的肠促胰岛素候选物。胃抑肽的释放取决于营养物质的吸收。因此，胃抑肽异常发生在大量胃肠道和代谢性疾病中。这些继发性变化很少具有临床意义。然而，胃抑肽分泌过多可能导致肥胖时脂肪生成增加以及晚期倾倒综合征时低血糖。在2型糖尿病中，已发现胃抑肽分泌过多和过少，但胃抑肽与胰岛素反应之间无相关性。胃抑肽异常与肠-胰岛轴紊乱并不相同。这些只能通过评估肠促胰岛素效应（比较口服葡萄糖的胰岛素反应与等血糖静脉注射葡萄糖的胰岛素反应）来评估。在空肠回肠旁路术患者和2型糖尿病患者中观察到肠促胰岛素效应降低。在这两种情况下，均未发现肠促胰岛素效应与胃抑肽反应之间存在相关性。得出的结论是，肠-胰岛轴紊乱很少由胃抑肽异常来解释。因此，必定存在其他体液性肠道因子。肠-胰岛轴的神经部分在健康和疾病状态下也需要探索。
