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低血糖、脑能量代谢与低血糖性神经元死亡。

Hypoglycemia, brain energetics, and hypoglycemic neuronal death.

作者信息

Suh Sang Won, Hamby Aaron M, Swanson Raymond A

机构信息

Department of Neurology, University of California, San Francisco, California, and.

Veterans Affairs Medical Center, San Francisco, California.

出版信息

Glia. 2007 Sep;55(12):1280-1286. doi: 10.1002/glia.20440.

DOI:10.1002/glia.20440
PMID:17659530
Abstract

Hypoglycemia is a common and serious problem among diabetic patients receiving treatment with insulin or other glucose-lowering drugs. Moderate hypoglycemia impairs neurological function, and severe hypoglycemia leads to death of selectively vulnerable neurons. Recent advances have shed new light on the underlying processes that cause neuronal death in hypoglycemia and the factors that may render specific neuronal populations especially vulnerable to hypoglycemia. In addition to its clinical importance, the pathophysiology of hypoglycemia is an indicator of the unique bioenergetic properties of the central nervous system, in particular the metabolic coupling of neuronal and astrocyte metabolism. This review will focus on relationships between bioenergetics and brain dysfunction in hypoglycemia, the neuronal cell death program triggered by hypoglycemia, and the role of astrocytes in these processes.

摘要

低血糖是接受胰岛素或其他降糖药物治疗的糖尿病患者中常见且严重的问题。中度低血糖会损害神经功能,而严重低血糖会导致选择性易损神经元死亡。最近的进展为低血糖导致神经元死亡的潜在过程以及可能使特定神经元群体特别易受低血糖影响的因素提供了新的线索。除了其临床重要性外,低血糖的病理生理学是中枢神经系统独特生物能量特性的一个指标,特别是神经元和星形胶质细胞代谢的代谢偶联。本综述将重点关注低血糖时生物能量学与脑功能障碍之间的关系、低血糖触发的神经元细胞死亡程序以及星形胶质细胞在这些过程中的作用。

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