Diabetes increases brain damage caused by severe hypoglycemia
Diabetes increases brain damage caused by severe hypoglycemia
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DOI：
10.1152/ajpendo.91041.2008
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发表时间：
2009-07-01
影响因子：
5.1
通讯作者：
Fisher, Simon J.
中科院分区：
文献类型：
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作者：
Bree, Adam J.;Puente, Erwin C.;Fisher, Simon J.
Bree AJ、Puente EC、Daphna-Iken D、Fisher SJ。糖尿病会增加严重低血糖引起的脑损伤。 Am J Physiol Endocrinol Metab 297：E194-E201，2009。首次发表于 2009 年 5 月 12 日； doi: 10.1152/ajpendo.91041.2008.-胰岛素引起的严重低血糖会导致脑损伤。待检验的假设是，糖尿病预示着严重低血糖发作后会出现更广泛的脑组织损伤。九周大的雄性链脲佐菌素糖尿病 (DIAB; n = 10) 或注射媒介物的对照 (CONT; n = 7) Sprague-Dawley 大鼠在清醒且不受约束的情况下接受高胰岛素 (0.2 U.kg(-1).min(-1)) 严重低血糖 (10-15 mg/dl) 钳夹。各组的严重低血糖深度和持续时间（1 小时）精确匹配（CONT 11 +/- 0.5 和 DIAB 12 +/- 0.2 mg/dl，P = 不显着）。在严重低血糖期间，两组中癫痫样活动的发作次数相同。一周后，组织学分析显示海马区域存在广泛的神经元损伤，尤其是齿状回和 CA1 区域，CA3 区域较少（P < 0.05），尽管各组之间的海马总损伤没有差异。然而，在皮层中，DIAB 大鼠的死亡神经元数量明显多于 CONT 大鼠（P < 0.05）（2.3 倍）。神经元损伤与癫痫样活动的发生之间存在很强的相关性（r(2) > 0.9）。对未经历严重低血糖的糖尿病大鼠（n = 5）和非糖尿病大鼠（n = 5）组进行的单独研究显示没有脑损伤。总之，在所研究的条件下，严重低血糖会导致皮层和海马内区域的脑损伤，并且损伤程度与非麻醉大鼠中癫痫样活动的存在密切相关。结论是，为了应对胰岛素引起的严重低血糖，糖尿病独特地增加了特定大脑区域对神经元损伤的脆弱性。
Bree AJ, Puente EC, Daphna-Iken D, Fisher SJ. Diabetes increases brain damage caused by severe hypoglycemia. Am J Physiol Endocrinol Metab 297: E194-E201, 2009. First published May 12, 2009; doi: 10.1152/ajpendo.91041.2008.-Insulin-induced severe hypoglycemia causes brain damage. The hypothesis to be tested was that diabetes portends to more extensive brain tissue damage following an episode of severe hypoglycemia. Nine-week-old male streptozotocin-diabetic (DIAB; n = 10) or vehicle-injected control (CONT; n = 7) Sprague-Dawley rats were subjected to hyperinsulinemic (0.2 U.kg(-1).min(-1)) severe hypoglycemic (10-15 mg/dl) clamps while awake and unrestrained. Groups were precisely matched for depth and duration (1 h) of severe hypoglycemia (CONT 11 +/- 0.5 and DIAB 12 +/- 0.2 mg/dl, P = not significant). During severe hypoglycemia, an equal number of episodes of seizure-like activity were noted in both groups. One week later, histological analysis demonstrated extensive neuronal damage in regions of the hippocampus, especially in the dentate gyrus and CA1 regions and less so in the CA3 region (P < 0.05), although total hippocampal damage was not different between groups. However, in the cortex, DIAB rats had significantly (2.3-fold) more dead neurons than CONT rats (P < 0.05). There was a strong correlation between neuronal damage and the occurrence of seizure-like activity (r(2) > 0.9). Separate studies conducted in groups of diabetic (n = 5) and nondiabetic (n = 5) rats not exposed to severe hypoglycemia showed no brain damage. In summary, under the conditions studied, severe hypoglycemia causes brain damage in the cortex and regions within the hippocampus, and the extent of damage is closely correlated to the presence of seizure-like activity in nonanesthetized rats. It is concluded that, in response to insulin-induced severe hypoglycemia, diabetes uniquely increases the vulnerability of specific brain areas to neuronal damage.