非酮症高渗性糖尿病昏迷的发病机制。

Pathogenesis of nonketotic hyperosmolar diabetic coma.

作者信息

Joffe B I, Goldberg R B, Krut L H, Seftel H C

出版信息

Lancet. 1975 May 10;1(7915):1069-71. doi: 10.1016/s0140-6736(75)91833-4.

Abstract

Two concepts are advanced to explain some fo the puzzling biochemical features found in nonketotic hyperosmolar diabetic coma. It is firstly suggested that an insulinised liver (reflecting residual beta-cell secretory activity) coexists with a diabetic periphery, thereby inactivating intrahepatic oxidation of incoming free fatty acids, which are directed largly along nonketogenic metabolic pathways such as triglyceride synthesis. This could account for the lack of hyperketonaemia. Secondly, it is hypothesised that within the liver enhanced neoglucogenesis occurs, due to the prevailing portal-vein into ratio of glucagon to insulin, and is mainly responsible for the development of massive hyperglycaemia.

摘要

提出了两个概念来解释非酮症高渗性糖尿病昏迷中一些令人费解的生化特征。首先有人认为，胰岛素作用的肝脏（反映残余β细胞分泌活动）与糖尿病外周组织共存，从而使进入肝脏的游离脂肪酸的肝内氧化失活，这些游离脂肪酸主要沿着非生酮代谢途径，如甘油三酯合成。这可以解释为何缺乏高酮血症。其次，有人假设，由于门静脉中胰高血糖素与胰岛素的比例占优势，肝脏内会发生增强的糖异生，这主要是导致大量高血糖的原因。