Suppr超能文献

胰岛素治疗可阻止叙利亚仓鼠由链脲佐菌素诱导的糖尿病自然恢复。一项放射自显影和免疫组织化学研究。

Insulin therapy prevents spontaneous recovery from streptozotocin-induced diabetes in Syrian hamsters. An autoradiographic and immunohistochemical study.

作者信息

Pour P M, Duckworth W, Carlson K, Kazakoff K

机构信息

Eppley Institute, University of Nebraska Medical Center, Omaha 68198.

出版信息

Virchows Arch A Pathol Anat Histopathol. 1990;417(4):333-41. doi: 10.1007/BF01605785.

Abstract

Streptozotocin (Sz) given as a single dose of 50 mg/kg body wt. caused severe diabetes in Syrian hamsters. However, the level of blood glucose decreased gradually after 21 days post-Sz and reached the near normal level at 70 days in 90% of hamsters. The recovery from diabetes was associated with the regeneration of the beta-cells of islets and a reduction in the initially increased number of alpha- and delta-cells. Daily treatment of diabetic hamsters with insulin was associated with the persistence of severe diabetes, lack of or minimal tendency for beta-cell regeneration and sustained hyperplasia of alpha- and delta-cells in 90% of hamsters. Insulin also inhibited DNA synthesis (as measured by incorporation of tritiated thymidine), in ductal, ductular and acinar cells in Sz-pretreated hamsters but not in normoglycemic control hamsters treated with insulin alone. The results demonstrate a deleterious effect of exogenous insulin in the course of Sz-induced diabetes in hamsters.

摘要

以50毫克/千克体重的单剂量给予链脲佐菌素(Sz)可导致叙利亚仓鼠患严重糖尿病。然而,在注射链脲佐菌素后21天,血糖水平逐渐下降,90%的仓鼠在70天时血糖水平接近正常。糖尿病的恢复与胰岛β细胞的再生以及最初增加的α细胞和δ细胞数量的减少有关。每天用胰岛素治疗糖尿病仓鼠,会导致严重糖尿病持续存在,90%的仓鼠β细胞缺乏再生或再生倾向极小,α细胞和δ细胞持续增生。胰岛素还抑制了经链脲佐菌素预处理的仓鼠的导管、小导管和腺泡细胞中的DNA合成(通过氚标记胸腺嘧啶核苷掺入法测量),但对单独用胰岛素治疗的血糖正常的对照仓鼠没有这种作用。结果表明外源性胰岛素在链脲佐菌素诱导的仓鼠糖尿病病程中具有有害作用。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验