rol studies, completely normal rats treated with the triple-drug regimen developed markedly increased blood glucose levels, reaching 250 mg/dl in only ten days. In addition, the blood insulin levels increased by three-fold, indicating that these normal rats had become insulin resistant as a result of the triple drug treatment. (Insulin resistance is the cause of Type 2 diabetes, commonly encountered in adults.) In the second, longer study, the control rats all remained diabetic throughout the study and died by week 18 with blood glucose levels in the
400 mg/dl range.
"We have demonstrated that using gene therapy strategies to deliver a growth factor, in this case HGF, to islet cells can improve the efficacy of portal pancreatic islet transplants over the long term using a model of juvenile, or Type 1, diabetes," said Dr. Stewart. "However, the fact that even the non-diabetic, non-transplanted control rats developed severe diabetes with the standard immunosuppressive drug therapy used following human islet cell transplants makes me wonder whether the same might not be occurring in humans, thereby increasing the number of islets needed for successful transplant outcomes and ultimately causing failure of islet grafts. These issues now need to be studied in humans."
"In brief, in my view, the Edmonton protocol for the transplantation of islets is a modern miracle. Our work suggests further optimism: there still may be room for further improvement,"
Dr. Stewart concluded.
The Edmonton Protocol to treat Type 1 diabetes was developed by researchers at the University of Alberta in Edmonton, Canada. Doctors use ultrasound to guide placement of a small catheter through the upper abdomen and into the liver. Pancreatic islet cells are then injected through the catheter into the liver. In time, islets are established in the liver and begin releasing insulin.
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Contact: Frank Raczkiewicz
RaczkiewiczFA@upmc.edu
412-647-3555
University of Pittsburgh Medical Center
4-Feb-2004
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