Vicent D, Garcia-Martinez J A, Villanueva-Peñacarrillo M L, Valverde I, Malaisse W J
Laboratory of Experimental Medicine, Brussels Free University, Belgium.
Diabetes Res Clin Pract. 1995 Jan;27(1):27-30. doi: 10.1016/0168-8227(94)01024-t.
The dimethyl ester of L-glutamic acid (GME) stimulates insulin release in isolated pancreatic islets and may represent a novel experimental tool in the study of non-insulin-dependent diabetes. In the present study, GME was found both to stimulate insulin secretion and to augment glibenclamide-stimulated insulin release in normal anaesthetized rats. A comparable hierarchy in the magnitude of the secretory response to GME and/or glibenclamide was found in control rats and animals injected with streptozotocin during the neonatal period. In the latter animals, however, the B-cell secretory response was invariably lower than in control animals. It is proposed that GME represents a novel tool to bypass anomalies of glucose transport and metabolism in the beta cell and, hence, to stimulate insulin release and enhance the insulinotropic action of hypoglycaemic sulphonylurea in animal models of non-insulin-dependent diabetes.
L-谷氨酸二甲酯（GME）可刺激分离的胰岛释放胰岛素，可能是研究非胰岛素依赖型糖尿病的一种新型实验工具。在本研究中，发现GME既能刺激正常麻醉大鼠的胰岛素分泌，又能增强格列本脲刺激的胰岛素释放。在对照大鼠和新生期注射链脲佐菌素的动物中，对GME和/或格列本脲的分泌反应强度具有相似的等级关系。然而，在后者动物中，B细胞分泌反应始终低于对照动物。有人提出，GME是一种新型工具，可绕过β细胞中葡萄糖转运和代谢的异常情况，从而在非胰岛素依赖型糖尿病动物模型中刺激胰岛素释放并增强降血糖磺酰脲类药物的促胰岛素作用。
