About 1 million people, between 5 percent and 10 percent of all diagnosed cases of diabetes, in the U.S. are affected by type 1 diabetes, for which there is no cure or preventive measure.
"This model allows us to get a transcriptional signature, a fingerprint, of how beta cells fend off the pharmaceutical stimulus we provide to prompt cell death," Dr. Scherer said. "In other words, it provides a way to identify the most critical factors that protect against beta cell death and to potentially find ways to increase these factors in people with type 1 diabetes."
The key, Dr. Scherer said, is that the process researchers use to kill beta cells is very targeted.
"It creates very little inflammation, so we can eliminate specific cells with minimal collateral damage," he said. "The other nice aspect is that we can do it in a very dose-dependent way, so we can ablate, or kill, just a few cells, or we can ablate almost all of them."
Dr. Scherer said this model lends itself to studying conditions of temporary hyperglycemia such as gestational diabetes, a condition in which pregnant women who have never had diabetes develop hyperglycemia. Gestational diabetes usually disappears after pregnancy, but it is not clear whether these transient bouts of elevated glucose can cause permanent damage in the vasculature that persists even after normal glucose levels have been restored.
Dr. Zhao Wang, a postdoctoral researcher at UT Southwestern and lead author of the study, said the strength of the PANIC-ATTAC mouse as a research tool lies partly in the ability to test how specific pharmaceuticals impact beta-cell regeneration.
"We can test which drugs can more rapidly repa
|Contact: Kristen Holland Shear|
UT Southwestern Medical Center