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糖尿病非酮症高渗性昏迷的病理生理学(作者译)

[Physiopathology of non-ketotic hyperosmolar coma in diabetes (author's transl)].

作者信息

Bataille C

出版信息

Diabete Metab. 1980 Dec;6(4):277-85.

PMID:7009249
Abstract

Hyperosmolar diabetic coma is characterised by extreme hyperglycaemia and dehydration. Hypernatremia often contributes additionally to plasma hyperosmolarity. The pathogenesis of these component abnormalities is considered. The explanation of the absence of hyperketonaemia is examined in the light of recent experimental and clinical data. At the beginning of the development of the syndrome, high peripheral plasma insulin probably explains the lack of ketosis via inhibition of lipolysis. Later, when hyperosmolar coma is established, peripheral insulinopenia but an "insulinised" liver may coexist. This would favour metabolism of free fatty acids along nonketogenic pathways.

摘要

高渗性糖尿病昏迷的特征是极度高血糖和脱水。高钠血症常常进一步加重血浆高渗状态。本文探讨了这些成分异常的发病机制,并根据最近的实验和临床数据研究了无高酮血症的原因。在该综合征发展初期,外周血浆胰岛素水平高可能通过抑制脂肪分解来解释酮血症的缺乏。后来,当高渗性昏迷确立时,外周胰岛素缺乏但肝脏处于“胰岛素化”状态可能同时存在。这将有利于游离脂肪酸沿非生酮途径代谢。

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