Miralles P, Peiró E, Dégano P, Silvestre R A, Marco J
Hospital Puerta de Hierro, Universidad Autonama de Madrid, Spain.
Diabetes. 1990 Aug;39(8):996-1001. doi: 10.2337/diab.39.8.996.
Results of studies on the effects of exogenous galanin on islet cell secretion are controversial. Until recently, only pig galanin has been available, and structural dissimilarities among the galanin molecules of different species might have contributed to discrepancies among the study results. Thus, we investigated the influence of synthetic rat galanin (50 nM) on unstimulated insulin, glucagon, and somatostatin release and on the responses of these hormones to arginine (10 mM), glucose (16.6 mM), and vasoactive intestinal polypeptide (VIP; 1 nM) in a homologous animal model, the perfused rat pancreas. In addition, the effect of an equimolar concentration of pig galanin on arginine-induced islet cell secretion was examined. Infusion of rat galanin reduced unstimulated insulin release (approximately 60%, P less than 0.01) and the insulin responses to arginine (approximately 30%, P less than 0.025), glucose (100%, P less than 0.01), and VIP (approximately 80%, P less than 0.025). Galanin also inhibited unstimulated somatostatin secretion (approximately 15%, P less than 0.05) and virtually abolished the somatostatin output evoked by arginine, glucose, and VIP. Conversely, rat galanin increased unstimulated glucagon output (approximately 20%, P less than 0.05), potentiated the glucagon response to arginine (approximately 50%, P less than 0.05) and VIP (approximately 90%, P less than 0.05), and counteracted the suppressor effect of glucose on alpha-cell secretion. Pig galanin inhibited the insulin output elicited by arginine (approximately 45%, P less than 0.05) but did not affect the somatostatin and glucagon responses to the aminogenic stimulus. In conclusion, the opposite effects of galanin on insulin and glucagon secretion favor the concept of galanin as a diabetogenic agent. Galanin also behaves as a potent inhibitor of somatostatin release. Finally, the importance of using homologous galanin to study the biological activity of this peptide must be emphasized.
关于外源性甘丙肽对胰岛细胞分泌影响的研究结果存在争议。直到最近,只有猪甘丙肽可用,不同物种的甘丙肽分子之间的结构差异可能导致了研究结果的差异。因此,我们在同源动物模型——灌注大鼠胰腺中,研究了合成大鼠甘丙肽(50 nM)对基础胰岛素、胰高血糖素和生长抑素释放的影响,以及这些激素对精氨酸(10 mM)、葡萄糖(16.6 mM)和血管活性肠肽(VIP;1 nM)的反应。此外,还检测了等摩尔浓度的猪甘丙肽对精氨酸诱导的胰岛细胞分泌的影响。输注大鼠甘丙肽可降低基础胰岛素释放(约60%,P<0.01)以及胰岛素对精氨酸(约30%,P<0.025)、葡萄糖(100%,P<0.01)和VIP(约80%,P<0.025)的反应。甘丙肽还抑制基础生长抑素分泌(约15%,P<0.05),并几乎完全消除精氨酸、葡萄糖和VIP引起的生长抑素分泌。相反,大鼠甘丙肽增加基础胰高血糖素分泌(约20%,P<0.05),增强胰高血糖素对精氨酸(约50%,P<0.05)和VIP(约90%,P<0.05)的反应,并抵消葡萄糖对α细胞分泌的抑制作用。猪甘丙肽抑制精氨酸诱导的胰岛素分泌(约45%,P<0.05),但不影响生长抑素和胰高血糖素对氨基酸刺激的反应。总之,甘丙肽对胰岛素和胰高血糖素分泌的相反作用支持了甘丙肽作为致糖尿病因子的概念。甘丙肽也是生长抑素释放的有效抑制剂。最后,必须强调使用同源甘丙肽来研究该肽生物活性的重要性。