Lambert D G, Atkins T W
Pharmaceutical Sciences Institute, Aston University, Birmingham.
J Endocrinol. 1989 Jun;121(3):479-85. doi: 10.1677/joe.0.1210479.
The effects of the islet cell hormones glucagon, somatostatin-28 and pancreatic polypeptide on insulin secretion from cultured cloned pancreatic B cells (HIT-T15 and RINm5F) have been investigated. Glucagon stimulates the secretion of insulin from HIT-T15 cells in the absence and presence of glucose and from RINm5F cells in the absence and presence of glyceraldehyde. HIT-T15 cells were more sensitive to the stimulatory effect of glucagon than RINm5F cells. Somatostatin-28 and pancreatic polypeptide, both alone and in combination, reduced glucose- and glucagon-stimulated insulin release from HIT-T15 cells and glyceraldehyde- and glucagon-stimulated insulin release from RINm5F cells. HIT-T15 cells were more sensitive to the inhibitory actions of somatostatin-28 and pancreatic polypeptide than RINm5F cells. This study supports the hypothesis that insulin release from normal B cells may be modified by the paracrine activity of islet hormones, glucagon, somatostatin and pancreatic polypeptide and probably occurs before any fine tuning imposed by subsequently released insulin.
已对胰岛细胞激素胰高血糖素、生长抑素 - 28和胰多肽对培养的克隆胰腺β细胞(HIT - T15和RINm5F)胰岛素分泌的影响进行了研究。在有无葡萄糖存在的情况下,胰高血糖素均可刺激HIT - T15细胞分泌胰岛素;在有无甘油醛存在的情况下,胰高血糖素均可刺激RINm5F细胞分泌胰岛素。HIT - T15细胞比RINm5F细胞对胰高血糖素的刺激作用更敏感。生长抑素 - 28和胰多肽单独或联合使用时,均可减少葡萄糖和胰高血糖素刺激的HIT - T15细胞胰岛素释放,以及甘油醛和胰高血糖素刺激的RINm5F细胞胰岛素释放。HIT - T15细胞比RINm5F细胞对生长抑素 - 28和胰多肽的抑制作用更敏感。本研究支持这样的假说,即正常β细胞的胰岛素释放可能受到胰岛激素、胰高血糖素、生长抑素和胰多肽旁分泌活性的调节,并且可能在随后释放的胰岛素进行任何微调之前就已发生。