Messier Claude
School of Psychology, University of Ottawa, 145 Jean-Jacques Lussier Room 352, Ottawa, Ontario, Canada K1N 6N5.
Eur J Pharmacol. 2004 Apr 19;490(1-3):33-57. doi: 10.1016/j.ejphar.2004.02.043.
The memory-improving action of glucose has now been studied for almost 20 years and the study of this phenomenon has led to a number of important developments in the understanding of memory, brain physiology and pathological consequences of impaired glucose tolerance. Glucose improvement of memory appears to involve two optimal doses in animals (100 mg/kg and 2 g/kg) that may correspond to two physiological mechanisms underlying glucose effects on memory. In humans, there have been few dose-response studies so the existence of more than one effective dose in humans is uncertain. Many tasks are facilitated by glucose in humans but tasks that are difficult to master or involve divided attention are improved more readily that easier tasks. There are a number of hypotheses about the physiological bases of the memory-improving action of glucose. Peripheral glucose injections could alleviate localized deficits in extracellular glucose in the hippocampus. These localized deficits may be due to changes in glucose transporters in that structure. Because certain neurotransmitters such as acetylcholine are directly dependent on the glucose supply for their synthesis, glucose is thought to facilitate neurotransmitter synthesis under certain circumstances. However, these hypotheses cannot account for the specificity of the dose-response effect of glucose. A number of peripheral mechanisms have been proposed, including the possibility that glucose-sensitive neurons in the brain or in the periphery may serve as glucose sensors and eventually produce neural changes that would facilitate memory processing. These latter results could be of importance because the mechanisms they suggest appear to be dose-dependent, a crucial characteristic to explain the dose-dependent effects of glucose. There may be an advantage to develop hypotheses that include both peripheral and central actions of glucose. There is evidence that impaired glucose regulation is associated with impaired cognition, particularly episodic memory. This impairment is minimal in young people but increases in older people (65 years and over) where it may compound other aging processes leading to reduced brain function. A small number of studies showed that glucose improvement of memory is associated with poor glucose regulation although this may not be the case for diabetic patients. Results of a few studies also suggest that drug treatments that improve glucose regulation also produce cognitive improvement in diabetic patients.
葡萄糖对记忆的改善作用现已研究了近20年，对这一现象的研究在记忆、脑生理学以及糖耐量受损的病理后果等方面的认识上带来了许多重要进展。在动物中，葡萄糖对记忆的改善似乎涉及两个最佳剂量（100毫克/千克和2克/千克），这可能对应于葡萄糖影响记忆的两种生理机制。在人类中，剂量反应研究较少，因此不确定人类是否存在不止一种有效剂量。在人类中，许多任务都因葡萄糖而得到促进，但难以掌握或涉及注意力分散的任务比简单任务更容易得到改善。关于葡萄糖改善记忆作用的生理基础有多种假说。外周注射葡萄糖可以缓解海马体中细胞外葡萄糖的局部不足。这些局部不足可能是由于该结构中葡萄糖转运体的变化所致。因为某些神经递质，如乙酰胆碱，其合成直接依赖于葡萄糖供应，所以认为葡萄糖在某些情况下有助于神经递质的合成。然而，这些假说无法解释葡萄糖剂量反应效应中的特异性。已经提出了一些外周机制，包括大脑或外周的葡萄糖敏感神经元可能作为葡萄糖传感器，并最终产生有助于记忆处理的神经变化。后一种结果可能很重要，因为它们所提示的机制似乎是剂量依赖性的，这是解释葡萄糖剂量依赖性效应的一个关键特征。提出同时包括葡萄糖外周和中枢作用的假说可能会有优势。有证据表明，葡萄糖调节受损与认知障碍有关，尤其是情景记忆障碍。这种障碍在年轻人中最小，但在老年人（65岁及以上）中会增加，在老年人中它可能会加剧其他衰老过程，导致脑功能下降。少数研究表明葡萄糖对记忆的改善与葡萄糖调节不良有关，尽管糖尿病患者可能并非如此。一些研究结果还表明，改善葡萄糖调节的药物治疗也能使糖尿病患者的认知得到改善。
