Sima Anders A F, Kamiya Hideki, Li Zhen Guo
Department of Pathology, Gordon H. Scott Hall of Basic Medical Sciences, Wayne State University, 540 East Canfield Avenue, Detroit, MI 48201, USA.
Eur J Pharmacol. 2004 Apr 19;490(1-3):187-97. doi: 10.1016/j.ejphar.2004.02.056.
Diabetes is an increasingly common disorder which causes and contributes to a variety of central nervous system (CNS) complications which are often associated with cognitive deficits. There appear to be two types of diabetic encephalopathy. Primary diabetic encephalopathy is caused by hyperglycemia and impaired insulin action, which evolves in a diabetes duration-related fashion and is associated with apoptotic neuronal loss and cognitive decline. This appears to be particularly associated with insulin-deficient diabetes. Secondary diabetic encephalopathy appears to arise from hypoxic-ischemic insults due to underlying microvascular disease or as a consequence of hypoglycemia. This type of cerebral diabetic complication is more common in the type 2 diabetic population. Here, we will review the clinical and experimental data supporting this conceptual division of diabetic CNS complications and discuss the underlying metabolic, molecular, and functional aberrations.
糖尿病是一种日益常见的疾病，它会引发并导致多种中枢神经系统（CNS）并发症，这些并发症常与认知缺陷相关。糖尿病性脑病似乎有两种类型。原发性糖尿病性脑病由高血糖和胰岛素作用受损引起，其发展与糖尿病病程相关，与神经元凋亡性损失和认知衰退有关。这似乎尤其与胰岛素缺乏型糖尿病相关。继发性糖尿病性脑病似乎源于潜在微血管疾病导致的缺氧缺血性损伤或低血糖的后果。这种类型的脑部糖尿病并发症在2型糖尿病患者中更为常见。在此，我们将回顾支持糖尿病中枢神经系统并发症这一概念性划分的临床和实验数据，并讨论潜在的代谢、分子和功能异常。
