Pácal Lukáš, Kuricová Katarína, Kaňková Kateřina
Lukáš Pácal, Katarína Kuricová, Kateřina Kaňková, Department of Pathophysiology, Faculty of Medicine, Masaryk University, 62500 Brno, Czech Republic.
World J Diabetes. 2014 Jun 15;5(3):288-95. doi: 10.4239/wjd.v5.i3.288.
Growing prevalence of diabetes (type 2 as well as type 1) and its related morbidity due to vascular complications creates a large burden on medical care worldwide. Understanding the molecular pathogenesis of chronic micro-, macro- and avascular complications mediated by hyperglycemia is of crucial importance since novel therapeutic targets can be identified and tested. Thiamine (vitamin B1) is an essential cofactor of several enzymes involved in carbohydrate metabolism and published data suggest that thiamine metabolism in diabetes is deficient. This review aims to point out the physiological role of thiamine in metabolism of glucose and amino acids, to present overview of thiamine metabolism and to describe the consequences of thiamine deficiency (either clinically manifest or latent). Furthermore, we want to explain why thiamine demands are increased in diabetes and to summarise data indicating thiamine mishandling in diabetics (by review of the studies mapping the prevalence and the degree of thiamine deficiency in diabetics). Finally, we would like to summarise the evidence for the beneficial effect of thiamine supplementation in progression of hyperglycemia-related pathology and, therefore, to justify its importance in determining the harmful impact of hyperglycemia in diabetes. Based on the data presented it could be concluded that although experimental studies mostly resulted in beneficial effects, clinical studies of appropriate size and duration focusing on the effect of thiamine supplementation/therapy on hard endpoints are missing at present. Moreover, it is not currently clear which mechanisms contribute to the deficient action of thiamine in diabetes most. Experimental studies on the molecular mechanisms of thiamine deficiency in diabetes are critically needed before clear answer to diabetes community could be given.
糖尿病（1型和2型）患病率不断上升及其因血管并发症导致的相关发病率给全球医疗保健带来了巨大负担。了解高血糖介导的慢性微血管、大血管和无血管并发症的分子发病机制至关重要，因为可以确定并测试新的治疗靶点。硫胺素（维生素B1）是参与碳水化合物代谢的几种酶的必需辅助因子，已发表的数据表明糖尿病患者的硫胺素代谢存在缺陷。本综述旨在指出硫胺素在葡萄糖和氨基酸代谢中的生理作用，概述硫胺素代谢，并描述硫胺素缺乏（无论是临床表现还是潜在表现）的后果。此外，我们想解释为什么糖尿病患者对硫胺素的需求会增加，并总结表明糖尿病患者硫胺素处理不当的数据（通过回顾绘制糖尿病患者硫胺素缺乏患病率和程度的研究）。最后，我们想总结硫胺素补充在高血糖相关病理进展中的有益作用的证据，从而证明其在确定高血糖对糖尿病有害影响方面的重要性。根据所提供的数据可以得出结论，尽管实验研究大多产生了有益效果，但目前缺乏针对硫胺素补充/治疗对硬终点影响的适当规模和持续时间的临床研究。此外，目前尚不清楚哪些机制对糖尿病中硫胺素作用不足的影响最大。在能够向糖尿病群体给出明确答案之前，迫切需要对糖尿病中硫胺素缺乏的分子机制进行实验研究。
