Hamming N A, Reynolds W A
Horm Metab Res. 1977 Mar;9(2):114-6. doi: 10.1055/s-0028-1093556.
The rates of DNA synthesis in islet and acinar cells were compared at different intervals following streptozotocin-induced diabetes. Streptozotocin, injected I.V. at a dosage of 65 mg/kg, consistently produced a diabetic-like state in young rats, ages 33 to 42 days. At two, four, and seven days after streptozotocin administration, no significant difference in DNA synthesis per mm2 of islet and acinar tissue was evident. However, four days after streptozotocin injection, a significant increase over control values was observed in the number of cells per islet incorporating tritiated thymidine. Following streptozotocin administration, beta cells generally appeared degranulated but not necrotic. Transformation of acinar cells or ductal elements to beta cells was not observed, suggesting that proliferating beta cells are the progeny of pre-existing beta cells. This study suggests that a brief, temporary period of compensatory proliferation of beta cells follows the initial insult of the diabetogenic agent streptozotocin in young rats.
在链脲佐菌素诱导的糖尿病模型中，于不同时间间隔比较胰岛细胞和腺泡细胞中的DNA合成速率。以65mg/kg的剂量静脉注射链脲佐菌素，可使33至42日龄的幼鼠持续呈现糖尿病样状态。在给予链脲佐菌素后的第2天、第4天和第7天，每平方毫米胰岛组织和腺泡组织的DNA合成无显著差异。然而，在注射链脲佐菌素4天后，每个胰岛中掺入氚标记胸腺嘧啶核苷的细胞数量相较于对照值显著增加。给予链脲佐菌素后，β细胞通常呈现脱颗粒状态，但未发生坏死。未观察到腺泡细胞或导管成分向β细胞的转化，这表明增殖的β细胞是已存在的β细胞的后代。本研究表明，在幼鼠中，致糖尿病药物链脲佐菌素的初始损伤后，β细胞会有一段短暂的、代偿性增殖的时期。
