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已经证明用链佐霉素(简称 STZ)可诱发小鼠产生低胰岛素糖尿病,本工作用外源性注射生长抑素(简称 SS)和用半胱胺特异性耗竭内源性 SS 的方法,观察 SS 对 STZ 糖尿病小鼠血清胰岛素的影响。在注射 STZ(60mg/kg,ip)前10min 分别皮下注射 1μg/kg,5μg/kg,10μg/kg 的 SS 可预防 STZ 诱发的血清低胰岛素作用,并呈剂量-效应关系。注射半胱胺(300mg/kg,SC)24h 后再连续5d 皮下注射半量半胱胺维持,胰腺组织匀浆中的 SS 含量经放免测定鉴定已基本被耗竭。在实验的第7,9,11,16d 胰腺 SS 含量仍然维持在比对照组为低的水平,给这种小鼠注射 STZ,其血清胰岛素降低程度比仅接受 STZ 小鼠的大,此外,给耗竭胰腺内 SS的小鼠注射不足以引起高血糖的 STZ 也引起了血糖大大升高。以上结果表明,不仅外源性 SS有预防链佐霉素诱发的小鼠低血清胰岛素发生的作用,胰腺组织中的内源性 SS 也可能是一个对胰岛 B 细胞起保护作用的因素。
It has been shown that streptozotocin (abbreviated as STZ) can induce mice to produce hypoglycemic diabetes. In this study, exogenous injection of somatostatin (SS) and cysteamine-specific endogenous SS depletion were observed Effect of SS on Serum Insulin in STZ Diabetic Mice. The subcutaneous injection of 1μg / kg, 5μg / kg and 10μg / kg SS at 10 minutes before injection of STZ (60mg / kg, ip) prevented STZ-induced hypolipidemic effect and showed a dose-response relationship. Cysteamine (300 mg / kg, SC) was injected 24 h after SCI and then remained for half a day for 5 days. The content of SS in pancreatic tissue homogenate was almost exhausted by radioimmunoassay. On the 7th, 9th, 11th and 16th day of the experiment, the pancreatic SS content remained at a lower level than that of the control group. The mice were injected with STZ and the serum insulin level was reduced more than that of STZ mice. In addition, STZ depletion of mice with SS in the pancreas by insufficient injection of high blood sugar also caused a significant increase in blood glucose. The above results show that not only exogenous SS can prevent streptozotocin-induced mouse low serum insulin, the endogenous SS in pancreatic tissue may also be a protective factor on islet B cells.