Tanaka R, Shima K, Sawazaki N, Matsuyama T, Kumahara Y, Yanaihara N
Endocrinol Jpn. 1980 Jun;27(3):343-8. doi: 10.1507/endocrj1954.27.343.
In order to ascertain whether insulin secretion is inhibited by insulin per se, the effect of exogenous rat insulin on basal and stimulated rat C-peptide reactivity (CPR) release was studied in the isolated perfused rat pancreas. The pancreas was perfused with a medium containing 20 or 200 ng/ml of rat insulin for a 20 min equilibration period and successively for a 25 to 30 min test period during which time glucose (300 mg/100 ml), tolbutamide (500 micrograms/ml), glucagon (500 ng/ml) or arginine (10 mM) was added as a secretagogue. The concentration of glucose in the basal medium was 60 mg/100 ml. Exogenous insulin did not significantly suppress the basal CPR secretion, nor did it cause a suppression of the peak value or incremental area of CPR while the pancreas was stimulated, but it rather augmented them. No inhibitory effect of exogenous insulin on the basal or stimulated CPR release was noticed in the present study.
为了确定胰岛素本身是否会抑制胰岛素分泌,我们在离体灌注的大鼠胰腺中研究了外源性大鼠胰岛素对基础和刺激状态下大鼠C肽反应性(CPR)释放的影响。用含有20或200 ng/ml大鼠胰岛素的培养基灌注胰腺20分钟以达到平衡期,随后进行25至30分钟的测试期,在此期间加入葡萄糖(300 mg/100 ml)、甲苯磺丁脲(500微克/ml)、胰高血糖素(500 ng/ml)或精氨酸(10 mM)作为促分泌剂。基础培养基中的葡萄糖浓度为60 mg/100 ml。外源性胰岛素并未显著抑制基础CPR分泌,在刺激胰腺时也未导致CPR峰值或增量面积的抑制,反而使其增加。在本研究中未观察到外源性胰岛素对基础或刺激状态下CPR释放的抑制作用。