Experimental drugs reduce neuron death in rats following insulin shock

In a study conducted in rats, scientists have determined that drugs that block the action of a group of DNA-repair enzymes can protect brain cells from damage triggered by an overdose of insulin. If these drugs are shown to produce the same effect in humans, they could become the first tool available for prevention of brain damage that can result from hypoglycemic shock, also known as insulin shock, in patients with diabetes. The study was conducted by scientists at the San Francisco Veterans Affairs Medical Center (SFVAMC) and appears in the November 19 issue of the Journal of Neuroscience.

The drugs, PARP inhibitors, have already been shown to protect human heart and brain cells from damage following heart attack and stroke, and are currently approved for testing in phase-2 clinical trials for victims of heart attack.

"Every hospital emergency department sees one or more cases of hypoglycemic coma each year," says Raymond Swanson, MD, chief of Neurology Service at SFVAMC and a professor in the Department of Neurology, University of California, San Francisco (UCSF.) "Up to this point, we don't have any way to treat these patients except to give them glucose, which pulls them out of insulin shock, but doesn't do anything to stop the cell death process that is triggered by severe hypoglycemia. PARP inhibitors rescue neurons [brain cells] which would otherwise go on to die even though blood glucose is restored."

About five to six million people in the United States take insulin to control diabetes, a chronic disease characterized by the body's impaired use or diminished production of insulin, a hormone produced in the pancreas that regulates glucose (sugar) levels in the blood. Diabetes patients monitor their blood sugar, often several times a day, and inject themselves with insulin to maintain appropriate blood sugar levels. However, calculating the correct dose of insulin can be difficult: The body's requirement changes depending on the cont

Contact: Liese Greensfelder
University of California - San Francisco

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