LIMITED B-CELL REGENERATION IN A B-CELL DEFICIENT RAT MODEL - STUDIES WITH DEXAMETHASONE
LIMITED B-CELL REGENERATION IN A B-CELL DEFICIENT RAT MODEL - STUDIES WITH DEXAMETHASONE
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DOI：
10.1016/0026-0495(81)90071-8
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发表时间：
1981-01-01
影响因子：
9.8
通讯作者：
WEIR, GC
中科院分区：
文献类型：
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作者：
BONNERWEIR, S;TRENT, DF;WEIR, GC
在2日龄给予链脲佐菌素（SZ）治疗的新生大鼠表现出短暂的高血糖，并伴有B细胞的再生，与正常血糖的恢复平行。在6周龄时，这些动物出现非酮症性高血糖，表明早期SZ治疗后B细胞再生不足且有限。为了测试该模型中B细胞的复制能力，尝试用药理学量的糖皮质激素地塞米松治疗13天来诱导额外的复制。地塞米松治疗导致sz治疗大鼠血浆葡萄糖显著升高（196 +-）。预处理23 mg/dl vs.预处理428。30毫克/分升处理后)，而不影响正常窝鼠。两组患者血浆胰岛素浓度均升高。在正常的非SZ大鼠中，糖皮质激素增加了胰腺胰岛素浓度，而在SZ组中，已经很低的胰岛素浓度没有增加。地塞米松使非SZ动物的B细胞/胰岛数量增加，但对SZ大鼠的B细胞减少数量没有增加。证据提供了一个限制的能力，B细胞复制在这个模型。至于其他胰岛肽，地塞米松没有引起血浆胰高血糖素浓度的显著变化。SZ大鼠胰高血糖素浓度降低，经糖皮质激素治疗后恢复正常。胰腺生长抑素浓度在非SZ组和SZ组中相似，在地塞米松治疗后两组均升高。糖皮质激素导致两组胃窦生长抑素浓度下降。地塞米松对胰腺和胃生长抑素浓度的影响是不同的。胰高血糖素和生长抑素组织含量变化的机制尚不清楚。
Neonatal rats treated with streptozotocin (SZ) at 2 days of age show a transient hyperglycemia with regeneration of B cells that parallels the recovery of normoglycemia. At 6 wk of age, these animals develop non-ketotic hyperglycemia, suggesting that the regeneration of B cells after the early SZ treatment was insufficient and limited. To test the replicative capacity of the B cells in this model, induction of additional replication was attempted with a 13 day treatment of pharmacological amounts of the glucocorticoid dexamethasone. Dexamethasone treatment led to a marked increase of plasma glucose in SZ-treated rats (196 .+-. 23 mg/dl pretreatment vs. 428 .+-. 30 mg/dl post-treatment), while not affecting that of the normal littermates. Plasma insulin concentrations were increased in both groups. Pancreatic insulin concentration was increased by the glucocorticoid in the normal non-SZ rats, whereas no increase in the already low insulin concentrations was found in the SZ group. Dexamethasone produced an increase in the B cell number/islet of the non SZ animals, but no increase in the reduced B cell number of the SZ rats. Evidence is provided for a limitation in the capacity for B cell replication in this model. With regard to other islet peptides, dexamethasone did not cause a significant change in plasma glucagon concentrations. Pancreatic glucagon concentration, which was reduced in the SZ rats, was normalized with glucocorticoid treatment. Pancreatic somatostatin concentration was similar in both the non-SZ and SZ groups, and increased following dexamethasone in both of these groups. Glucocorticoid led to a fall in the somatostatin concentration of the gastric antrum in both groups. The effects of dexamethasone upon pancreatic and gastric somatostatin concentrations are divergent. The mechanisms responsible for the changes in glucagon and somatostatin tissue content remain unclear.