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.
中科院分区:
文献类型:
--
作者:
Canada, Sarah E.;Weaver, Staci A.;Sharpe, Shannon N.;Pederson, Bartholomew A.
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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