Diabetes Publish Ahead of Print published online ahead of print April 24, 2007 DOI: 10.2337/db06-1385
Hematopoietic Stem Cells Derived from Adult Donors are Not a Source of Pancreatic Beta Cells in Adult Non Diabetic Humans
Alexandra E Butler1,
Andrew Huang1,
P. Nagesh Rao2,
Anil Bhushan1,
William J. Hogan3,
Robert A Rizza4, and
Peter C Butler1
Larry Hillblom Islet Research Center1
Pathology and Laboratory Medicine2, UCLA, Los Angeles, CA.
Division of Hematology3, Mayo Clinic, Rochester, MN, USA
Division of Endocrinology, Diabetes, Metabolism and Nutrition4, Mayo Clinic, Rochester, MN, USA
Objective.: Type 1 and type 2 diabetes are characterized respectively by 98% and 65% loss of pancreatic ß-cells. Efforts to reverse either form of diabetes increasingly focus on the possibility of promoting ß-cell replacement and/or regeneration. Islet transplantation has been explored, but does not provide long-term insulin independence. One possible source of ß-cell regeneration is hematopoietic stem cells. In mice there are conflicting data as to whether hematopoietic stem cells contribute to pancreatic ß-cells. We sought to establish if hematopoietic stem cells (derived from adult donors) transdifferentiate into pancreatic beta cells in adult humans.
Research Design and Methods.: We addressed this in 31 human pancreases obtained at autopsy from hematopoietic stem cell transplant recipients who had received their transplant from a donor of the opposite gender.
Results.: While some donor derived cells were observed in the non-endocrine pancreas, no pancreatic beta cells were identified that were derived from donor hematopoietic stem cells, including two cases with type 2 diabetes.
Conclusions.: We conclude that hematopoietic stem cells derived from adult donors contribute minimally to pancreatic beta cells in non-diabetic adult humans. These data do not rule out the possibility that hematopoietic stem cells contribute to pancreatic beta cells in childhood or in people with type 1 diabetes.

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J. J. Meier, A. E. Butler, Y. Saisho, T. Monchamp, R. Galasso, A. Bhushan, R. A. Rizza, and P. C. Butler
{beta}-Cell Replication Is the Primary Mechanism Subserving the Postnatal Expansion of {beta}-Cell Mass in Humans
Diabetes,
June 1, 2008;
57(6):
1584 - 1594.
[Abstract]
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Copyright © 2007 by the American Diabetes Association.
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