Ipp E, Garberoglio C, Richter H, Moossa A R, Rubenstein A H
Diabetes. 1984 Jul;33(7):619-21. doi: 10.2337/diab.33.7.619.
Intracerebroventricular (ICV) instillation of morphine and beta-endorphin causes centrally induced hyperglycemia. Locally active, endogenous opioids in the central nervous system may, therefore, also be involved in the elevation of blood sugar. This possibility was tested by examining the glucoregulatory response to central glucoprivation induced by ICV administration of 2-deoxy-D-glucose (2DG) in dogs. Administration of 2DG resulted in a rise in plasma glucose and immunoreactive glucagon (IRG) of 108 +/- 19 mg/dl and 70 +/- 20 pg/ml, respectively. These changes were attenuated by the simultaneous central infusion of the opiate antagonist naloxone: plasma glucose levels increased by 77 +/- 14 mg/dl and IRG by 43 +/- 3 pg/ml, both significantly different from the effect of 2DG alone (P less than 0.05-0.01). These findings suggest that opiate receptors participate in the counterregulatory response to central glucoprivation. They also provide a mechanism by which endogenous opioid peptides may play a role in the central regulation of glucose homeostasis.
脑室内（ICV）注射吗啡和β-内啡肽会引起中枢性高血糖。因此，中枢神经系统中具有局部活性的内源性阿片类物质可能也与血糖升高有关。通过检测犬脑室内注射2-脱氧-D-葡萄糖（2DG）诱导中枢性糖剥夺后糖调节反应，对这一可能性进行了测试。注射2DG后，血浆葡萄糖和免疫反应性胰高血糖素（IRG）分别升高了108±19mg/dl和70±20pg/ml。同时脑室内输注阿片拮抗剂纳洛酮可减弱这些变化：血浆葡萄糖水平升高77±14mg/dl，IRG升高43±3pg/ml，两者均与单独使用2DG的效果有显著差异（P<0.05-0.01）。这些发现表明，阿片受体参与了对中枢性糖剥夺的对抗调节反应。它们还提供了一种机制，通过该机制内源性阿片肽可能在葡萄糖稳态的中枢调节中发挥作用。
