The researchers first injected rats with a drug that kills pancreatic beta cells in order to mimic human insulin-dependent, or juvenile, diabetes (type 1), a condition in which beta cells are unable to produce insulin. They then transplanted beta cells into the animals livers. Fat accumulations were found around islets four weeks after transplantation. Insulin levels declined, and the animals died at 15 weeks.
Another group of similar rats was then exposed to one of two conditions that reduce body fat a restricted diet or administration of leptin, a hormone that decreases appetite and increases metabolism. In both cases, more beta cells survived. Rats that had received leptin also showed the highest survival rate of beta cells.
Because the differences among the groups of rats could be traced to the amount of fat, and no anti-rejection drugs had been given, the results validate their theory that fat was the culprit in killing the beta cells, Dr. Unger said.
These results also suggest that diet and weight control might enable transplanted beta cells in humans to survive longer or avoid destruction, he said.
This seems very easy to prevent, but its not being targeted by researchers, he said.
Dr. Unger said the study could also serve as a model for death of beta cells in non-insulin-dependent, or adult-onset, diabetes (type 2), a condition that is associated largely with obesity. His group is now working with other researchers at UT Southwestern to determine if excess fat is killing cells in obese humans.
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| Contact: Aline McKenzie aline.mckenzie@utsouthwestern.edu 214-648-3404 UT Southwestern Medical Center Source:Eurekalert |