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Glucose Triggers Brain Damage After Hypoglycemic Coma: Study

Work with rats shows damage happened in effort to normalize blood sugar levels


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FRIDAY, April 13 (HealthDay News) -- Glucose administered to treat hypoglycemic coma -- not the coma itself -- caused brain damage in rats, a new study found.

The results surprised the San Francisco VA Medical Center researchers, who said the findings may be of clinical significance for the treatment of diabetics in hypoglycemic coma. However, the researchers added that these findings in rats do not necessarily apply to humans.

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People in hypoglycemic coma -- caused by extremely low blood glucose levels -- can suffer destruction of neurons in the hippocampus and cerebral cortex, areas of the brain that are essential to memory and cognition.

"This study tells us for the first time that, in rats, the brain damage occurs not during the coma, but after it, when we give them glucose and their blood glucose levels return to normal," principal investigator Dr. Raymond A. Swanson, chief of the neurology and rehabilitation service at the veterans' center, said in a prepared statement.

He and his colleagues also identified how the brain damage occurs. The sudden return of glucose to the brain activates the enzyme NADPH oxidase, which triggers a process of oxidative stress that kills neurons.

The study is published in the April issue of the Journal of Clinical Investigation.

"The rats could remain hypoglycemic without evidence of significant oxidative stress for at least 60 minutes. It was only when we gave them glucose to reverse the hypoglycemia that the oxidative stress occurred. This was a real surprise," said Swanson, who is also professor and vice chairman of neurology at the University of California, San Francisco.

More information

The U.S. National Diabetes Information Clearinghouse has more about hypoglycemia.



-- Robert Preidt

Copyright © 2007 ScoutNews, LLC. All rights reserved.
Last updated 4/13/2007

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SOURCE: University of California, San Francisco, news release, April 4, 2007


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