Pathophysiologic mechanisms of postprandial hyperglycemia
Pathophysiologic mechanisms of postprandial hyperglycemia
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DOI：
10.1016/s0002-9149(01)01830-6
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发表时间：
2001-09-20
影响因子：
2.8
通讯作者：
Gavin, JR III
中科院分区：
文献类型：
--
作者：
Gavin, JR III
餐后高血糖在糖尿病相关并发症和预后的病因中的作用，尽管仍在阐明，但比之前认为的更大。进食后的急性血糖升高与各种葡萄糖介导的组织缺陷相关--氧化应激、糖基化和晚期糖基化最终产物的形成--这些缺陷对几乎每个人体器官系统都有深远的结构和功能后果。只有通过降低餐后和空腹血糖水平，才能将糖化血红蛋白降低到预防或延缓这些并发症的水平。α-葡萄糖苷酶抑制剂(阿卡波糖、伏格列波糖、米格列醇)有效地延缓了碳水化合物的消化和吸收，从而在不损失卡路里的情况下减少了餐后血糖水平的激增。然而，需要更加重视餐后血糖的测量，以便读数可以用来指导治疗。(C)2001年，由Excerpta Medica，Inc.
The role of postprandial hyperglycemia in the etiology of diabetes-related complications and outcomes, although still being elucidated, is greater than previously thought. Acute glucose elevations after meal ingestion are associated with a variety of glucose-mediated tissue defects-oxidative stress, glycation, and advanced glycation end product formation-which have far-reaching structural and functional consequences for virtually every human organ system. Lowering glycosylated hemoglobin to levels that prevent or delay these complications can be achieved only by reducing both postprandial and fasting plasma glucose levels. The a-glucosidase inhibitors (acarbose, voglibose, miglitol) have been effective in delaying the digestion and absorption of carbohydrates, thus diminishing the postprandial surge in blood glucose levels without loss of calories. However, greater emphasis needs to be placed on the measurement of postprandial glycemia, so that readings can be used to guide treatment. (C) 2001 by Excerpta Medica, Inc.