Mouse model developed at UT Southwestern mimics hyperglycemia, aids in diabete...( DALLAS June 2 2008 UT Southwestern...)

DALLAS June 2, 2008 UT Southwestern Medical Center researchers have genetically engineered a laboratory mouse in which pancreatic beta cells can regenerate after being induced to die. The new animal model's regenerative ability may provide future insights into improved treatments of diabetes, which affects millions of Americans.

The model, named the PANIC-ATTAC mouse, mimics what occurs in humans with type 1 diabetes, a condition that develops when the body's immune system destroys pancreatic beta cells, as well as in type 2 diabetes, where beta cells die from working overtime.

After inducing death in the beta cells which make and release the hormone insulin the researchers found that the engineered mice's beta-cell populations can regenerate, which makes the animal useful for studying conditions such as type 1 diabetes, hyperglycemia (high blood sugar) and gestational diabetes.

The animal model is described online and in a future print issue of the journal Diabetes.

"The ability to induce cell death is not novel. The fact that the beta cells regenerate after we kill them is really the new aspect of the model," said Dr. Philipp Scherer, professor of internal medicine, director of the Touchstone Center for Diabetes Research at UT Southwestern and senior author of the study. "It enables us to see what kind of event or pharmacological intervention might stimulate or enhance the regeneration."

In the study, the researchers genetically manipulated mature, insulin-positive pancreatic beta cells in the PANIC-ATTAC mice so that these cells would die when they came in contact with a drug. When the researchers stopped administering the drug and allowed the animals to recover, they found that the animals' beta cells had regenerated and their blood glucose levels returned to normal after two months.

Dr. Scherer said it's unclear what caused the pancreatic beta cells to regenerate, but uncovering the
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