Brain glycogen supercompensation in the mouse after recovery from insulin-induced hypoglycemia.

Brain glycogen supercompensation in the mouse after recovery from insulin-induced hypoglycemia.
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DOI:
10.1002/jnr.22579
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发表时间:
2011-04
影响因子:
4.2
通讯作者:
Pederson, Bartholomew A.
Pederson, Bartholomew A.
中科院分区:
医学3区
文献类型:
--
作者:
Canada, Sarah E.;Weaver, Staci A.;Sharpe, Shannon N.;Pederson, Bartholomew A.

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脑糖原被认为在生理和病理条件下都起作用。假设大脑中这种葡萄糖聚合物的药理学升高可以保护神经元免受低血糖诱导的细胞死亡。在接受胰岛素治疗的糖尿病患者中,由于先前的低血糖导致的脑糖原水平升高被认为是导致低血糖相关自主神经功能衰竭(HAAF)的原因。后一种升高糖原水平的模式被称为“超补偿”。我们测试了在从胰岛素诱导的急性或复发性低血糖恢复后,健康清醒的小鼠是否发生脑糖原超补偿。通过给予胰岛素将血糖水平降低至低于2.2 mmol/L,持续90 min。急性或复发性低血糖发作后,脑葡萄糖水平至少降低80%,脑糖原水平降低约50%。在这些低血糖发作后,允许小鼠进食6或27小时。6小时后,与盐水处理的对照组相比,先前经历急性或复发性低血糖的小鼠的血液和脑葡萄糖水平恢复,而脑糖原水平升高25%。经过27小时的恢复期后,先前经历急性或复发性低血糖的小鼠的脑糖原浓度已恢复至基线水平。我们的结论是,脑糖原超补偿发生在健康小鼠,但其功能意义仍有待确定。
Brain glycogen is proposed to function in both physiological and pathological conditions. Pharmacological elevation of this glucose polymer in brain is hypothesized to protect neurons against hypoglycemia-induced cell death. Elevation of brain glycogen levels due to prior hypoglycemia is postulated to contribute to the development of hypoglycemia-associated autonomic failure (HAAF) in insulin-treated diabetic patients. This latter mode of elevating glycogen levels is termed “supercompensation”. We tested whether brain glycogen supercompensation occurs in healthy, conscious mice after recovery from insulin-induced acute or recurrent hypoglycemia. Blood glucose levels were lowered to less than 2.2 mmol/L for 90 min by administration of insulin. Brain glucose levels decreased at least 80% and brain glycogen levels decreased approximately 50% after episodes of either acute or recurrent hypoglycemia. Following these hypoglycemic episodes, mice were allowed access to food for 6 or 27 hrs. After 6 hrs, blood and brain glucose levels were restored while brain glycogen levels were elevated 25% in mice that were previously subjected to either acute or recurrent hypoglycemia as compared with saline-treated controls. Following a 27 hr recovery period, the concentration of brain glycogen had returned to baseline levels in mice previously subjected to either acute or recurrent hypoglycemia. We conclude that brain glycogen supercompensation occurs in healthy mice but its functional significance remains to be established.
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