Setter Stephen M, Campbell R Keith, Cahoon Clifton J
Department of Pharmacotherapy, College of Pharmacy, Washington State University/Elder Services, Spokane, WA, USA.
Ann Pharmacother. 2003 Dec;37(12):1858-66. doi: 10.1345/aph.1D002.
To review the current biochemical theories on how diabetes contributes to microvascular disease.
MEDLINE search (1980-June 2003) and bibliographies of articles obtained on this topic.
Articles identified from the data sources were evaluated and those deemed relevant to this review were incorporated.
The prevailing biochemical theories on how diabetes leads to microvascular disease include increased polyol (sorbitol/aldose reductase) pathway flux, production of advanced glycation end-products, generation of reactive oxygen species, and activation of diacylglycerol and protein kinase C isoforms. These pathways contribute to endothelial damage and dysfunction and may alter gene functioning.
Each pathway, via varied and often overlapping mechanisms, contributes to altered microvascular function that leads to the development of retinopathy, neuropathy, and nephropathy, the major microvascular complications associated with diabetes.
回顾当前关于糖尿病如何导致微血管疾病的生化理论。
医学在线数据库检索（1980年 - 2003年6月）以及关于该主题文章的参考文献。
对从资料来源中识别出的文章进行评估，并纳入那些被认为与本综述相关的文章。
关于糖尿病如何导致微血管疾病的主流生化理论包括多元醇（山梨醇/醛糖还原酶）途径通量增加、晚期糖基化终产物的产生、活性氧的生成以及二酰基甘油和蛋白激酶C亚型的激活。这些途径导致内皮损伤和功能障碍，并可能改变基因功能。
每条途径通过不同且常常相互重叠的机制，导致微血管功能改变，进而引发视网膜病变、神经病变和肾病，这些是与糖尿病相关的主要微血管并发症。
