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Diabetes 54:3205-3211, 2005
© 2005 by the American Diabetes Association, Inc.

Islet Cell Hormonal Responses to Hypoglycemia After Human Islet Transplantation for Type 1 Diabetes

Michael R. Rickels1, Mark H. Schutta1, Rebecca Mueller1, James F. Markmann2, Clyde F. Barker2, Ali Naji2, and Karen L. Teff1,3

1 Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania
2 Division of Transplantation, Department of Surgery, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania
3 Monell Chemical Senses Center, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania

Islet transplantation can eliminate severe hypoglycemic episodes in patients with type 1 diabetes; however, whether intrahepatic islets respond appropriately to hypoglycemia after transplantation has not been fully studied. We evaluated six islet transplant recipients, six type 1 diabetic subjects, and seven nondiabetic control subjects using a stepped hyperinsulinemic-hypoglycemic clamp. Also, three islet transplant recipients and the seven control subjects underwent a paired hyperinsulinemic-euglycemic clamp. In response to hypoglycemia, C-peptide was similarly suppressed in islet transplant recipients and control subjects and was not detectable in type 1 diabetic subjects. Glucagon was significantly more suppressed in type 1 diabetic subjects than in islet transplant recipients (P < 0.01), although the glucagon in islet transplant recipients failed to activate as in the control subjects (P < 0.01). Pancreatic polypeptide failed to activate in both type 1 diabetic subjects and islet transplant recipients compared with control subjects (P < 0.01). In islet transplant recipients, glucagon was suppressed normally by hyperinsulinemia during the euglycemic clamp and was significantly greater during the paired hypoglycemic clamp (P < 0.01). These results suggest that after islet transplantation and in response to insulin-induced hypoglycemia, endogenous insulin secretion is appropriately suppressed and glucagon secretion may be partially restored.

Address correspondence and reprint requests to Michael R. Rickels, MD, Division of Endocrinology, Diabetes & Metabolism, University of Pennsylvania School of Medicine, 778 Clinical Research Building, 415 Curie Blvd., Philadelphia, PA 19104-6149. E-mail: rickels{at}mail.med.upenn.edu

Abbreviations: HUP, Hospital of the University of Pennsylvania


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Copyright © 2005 by the American Diabetes Association.