"The mice bred to produce excess Akt1 protein were more tolerant of glucose and more resistant to diabetes in fact, we simply could not give them diabetes when we tried," said Morris J. Birnbaum, MD, PhD, associate director of the Penn Diabetes Center in the Penn Departments of Medicine & Cell and Molecular Biology and an investigator in the Howard Hughes Medical Institute. "The increase in Akt1 directly leads to an increase in the size, amount, and total production of insulin by β cells."
In the United States, diabetes is the seventh leading cause of death and currently effects over 15 million people. Medical science recognizes two forms of diabetes. Type 1 diabetes results from the immune systems destruction of pancreatic β cells. Type 2 diabetes results when the body cannot either produce enough insulin or properly use the insulin it does produce. Without insulin, the body cannot utilize glucose blood sugar which can lead to a variety of debilitating illnesses, including heart disease, blindness, and kidney failure.
Recently, surgeons have met with success in treating the disorder by transplanting clusters of pancreatic cells, called islets, into diabetic patients. Transplanted islets, which include β cells, have been shown to reestablish the production of insulin in the pancreas. Unfortunately, the demand for islets far outweighs the supply.
"What makes our findings so interesting, clinically, is the potential to enlarge our pool of β cells f
Contact: Greg Lester
University of Pennsylvania School of Medicine