Olsson S E, Anderson A, Petersson B, Hellerström C
Diabete Metab. 1976 Dec;2(4):199-202.
The glucose-stimulated insulin release of pancreatic islets isolated either from normal mice or from mice with the obese-hyperglycemic syndrome (genotype ob/ob) was inhibited by somatostatin in the concentration range 10(-2) - 10(-4) mM. Islets prepared from the obese-hyperglycemic mice appeared most sensitive and there was a strong inhibitory action on the insulin release irrespective of whether the islets were exposed to somatostatin directly after isolation or after five days in tissue culture. There was, however, no effect of somatostatin on the glucose-stimulated insulin biosynthesis of the mouse islets. Neither was there an effect on the insulin biosynthesis of isolated islets from three days old rats, despite a previous report to the contrary. It is concluded that somatostatin does not affect the insulin biosynthesis of isolated islets at concentrations which inhibit insulin release.
从正常小鼠或肥胖 - 高血糖综合征(基因型ob/ob)小鼠分离的胰岛,在10^(-2) - 10^(-4) mM浓度范围内,生长抑素可抑制其葡萄糖刺激的胰岛素释放。从肥胖 - 高血糖小鼠制备的胰岛似乎最为敏感,无论胰岛在分离后直接还是在组织培养5天后暴露于生长抑素,对胰岛素释放均有强烈的抑制作用。然而,生长抑素对小鼠胰岛葡萄糖刺激的胰岛素生物合成没有影响。尽管之前有相反的报道,但生长抑素对3日龄大鼠分离胰岛的胰岛素生物合成也没有影响。结论是,在抑制胰岛素释放的浓度下,生长抑素不影响分离胰岛的胰岛素生物合成。