MONDAY, Sept. 10 (HealthDay News) -- A new mouse model of diabetes suggests that insulin-producing pancreatic cells have the capacity to regenerate and reverse diabetes, and immunosuppressants used in human islet transplantation may block this regeneration, according to research published in the September issue of the Journal of Clinical Investigation.
Yuval Dor, Ph.D., from the Hebrew University-Hadassah Medical School in Jerusalem, Israel, and colleagues generated mice whose pancreatic islet beta cells could be selectively killed by a toxin after administering doxycycline.
The researchers found that the toxin led to the death of 70 percent to 80 percent of beta cells, destruction of islet architecture, and diabetes. Withdrawing doxycycline normalized blood glucose levels and led to substantial regeneration of beta cell mass, which was due to enhanced growth of the surviving beta cells. They note that two immunosuppressants used in the Edmonton protocol for human islet transplantation, sirolimus and tacrolimus, actually blocked beta cell regeneration and normalization of blood glucose.
"The results presented here show that pancreatic beta cells have a significant capacity for spontaneous regeneration, sufficient for recovery from overt diabetes," Dor and colleagues conclude. "This contrasts with the failure of beta cell regeneration in both autoimmune and pharmacological models of diabetes, which has led to the common perception that beta cells have a poor or non-existent regenerative capacity."
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