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脑心肌炎病毒诱导小鼠患糖尿病:胰岛结构和功能的长期变化

Encephalomyocarditis virus induced diabetes mellitus in mice: long-term changes in the structure and function of islets of Langerhans.

作者信息

Iwo K, Bellomo S C, Mukai N, Craighead J E

出版信息

Diabetologia. 1983 Jul;25(1):39-44. doi: 10.1007/BF00251895.

Abstract

Adult male mice infected with the M variant of encephalomyocarditis virus develop hyperglycaemia acutely as a consequence of B cell injury. The severity of the metabolic disease is variable and many animals become normoglycaemic during convalescence. The islets of Langerhans of these mice exhibit minor structural changes, but there are no significant abnormalities of insulin and glucagon secretion. In contrast, animals with persistent hyperglycaemia exhibit striking morphological alterations in the islets. The A cell mass is prominent, whereas B cells are reduced in number and exhibit striking cytological features. These changes are associated with both hypoinsulinaemia and hyperglucagonaemia.

摘要

感染脑心肌炎病毒M变种的成年雄性小鼠会因B细胞损伤而急性发生高血糖症。代谢性疾病的严重程度各不相同,许多动物在恢复期血糖恢复正常。这些小鼠的胰岛显示出轻微的结构变化,但胰岛素和胰高血糖素分泌没有明显异常。相比之下,持续高血糖的动物胰岛出现显著的形态学改变。A细胞团突出,而B细胞数量减少并呈现出显著的细胞学特征。这些变化与低胰岛素血症和高胰高血糖素血症均有关。

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