Giroix M H, Zhang T M, Leclercq-Meyer V, Sener A, Portha B, Malaisse W J
Laboratoire de Physiopathologie de la Nutrition, URA CNRS 307, University Denis Diderot (Paris VII), France.
Acta Diabetol. 1995 Oct;32(3):198-202. doi: 10.1007/BF00838492.
Pancreatic islets isolated from control rats, Goto-Kakizaki rats and adult rats that were injected with streptozotocin during the neonatal period were incubated for two successive period of 90 min each in the presence of D-glucose (11.1 mM) with or without formycin A (1.0 mM), and in the presence of the dimethyl ester of succinic acid (SAD, 10.0 mM) with or without palmitate (1.0 mM). Although formycin A augmented glucose-stimulated insulin release in both control and diabetic rats, it failed to compensate for the impaired secretory response to D-glucose in the latter animals. Likewise, non-glucidic nutrients such as SAD and/or palmitate failed to display a more efficient insulinotropic action, relative to basal insulin output, in diabetic than control rats. These results indicate that both formycin A and non-glucidic nutrients are unable, through their immediate insulinotropic action, to restore a normal output of insulin in islets of animals with inherited or acquired non-insulin-dependent diabetes.
从对照大鼠、Goto-Kakizaki大鼠以及新生期注射链脲佐菌素的成年大鼠分离出胰岛，分别在存在或不存在阿霉素A（1.0 mM）的情况下，于含D-葡萄糖（11.1 mM）的环境中连续孵育两个90分钟时间段；并在存在或不存在棕榈酸酯（1.0 mM）的情况下，于含琥珀酸二甲酯（SAD，10.0 mM）的环境中孵育。尽管阿霉素A增强了对照大鼠和糖尿病大鼠中葡萄糖刺激的胰岛素释放，但它未能弥补后者对D-葡萄糖分泌反应受损的情况。同样，相对于基础胰岛素分泌量，诸如SAD和/或棕榈酸酯等非糖类营养物质在糖尿病大鼠中并未比对照大鼠表现出更有效的促胰岛素作用。这些结果表明，阿霉素A和非糖类营养物质均无法通过其直接的促胰岛素作用，使遗传性或获得性非胰岛素依赖型糖尿病动物胰岛中的胰岛素输出恢复正常。
