Department of Veterinary Disease Biology, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark; Department of Diabetes Toxicology and Safety Pharmacology, Novo Nordisk A/S, Maaloev, Denmark.
J Neuroendocrinol. 2014 Mar;26(3):123-50. doi: 10.1111/jne.12133.
Insulin-induced hypoglycaemia (IIH) is a major acute complication in type 1 as well as in type 2 diabetes, particularly during intensive insulin therapy. The brain plays a central role in the counter-regulatory response by eliciting parasympathetic and sympathetic hormone responses to restore normoglycaemia. Brain glucose concentrations, being approximately 15-20% of the blood glucose concentration in humans, are rigorously maintained during hypoglycaemia through adaptions such as increased cerebral glucose transport, decreased cerebral glucose utilisation and, possibly, by using central nervous system glycogen as a glucose reserve. However, during sustained hypoglycaemia, the brain cannot maintain a sufficient glucose influx and, as the cerebral hypoglycaemia becomes severe, electroencephalogram changes, oxidative stress and regional neuronal death ensues. With particular focus on evidence from experimental studies on nondiabetic IIH, this review outlines the central mechanisms behind the counter-regulatory response to IIH, as well as cerebral adaption to avoid sequelae of cerebral neuroglycopaenia, including seizures and coma.
胰岛素诱导的低血糖（IIH）是 1 型和 2 型糖尿病的主要急性并发症，特别是在强化胰岛素治疗期间。大脑在通过引发副交感神经和交感神经激素反应来恢复正常血糖水平的代偿性反应中起着核心作用。大脑葡萄糖浓度在人类中约为血糖浓度的 15-20%，通过增加脑葡萄糖转运、减少脑葡萄糖利用等适应机制，在低血糖期间得到严格维持，并且可能利用中枢神经系统糖原作为葡萄糖储备。然而，在持续低血糖期间，大脑无法维持足够的葡萄糖流入，并且随着脑低血糖变得严重，脑电图改变、氧化应激和区域性神经元死亡随之发生。本综述特别关注非糖尿病性 IIH 的实验研究证据，概述了 IIH 代偿性反应背后的中枢机制，以及大脑适应以避免脑神经低血糖的后遗症，包括癫痫发作和昏迷。
