Translated title of the contribution: Pancreas transplant function in humans undergoing metabolic stress

A. U. Teuscher, E. R. Seaquist, Z. Barrou, D. M. Kendall, R. P. Robertson

Research output: Contribution to journalArticlepeer-review

1 Scopus citations


Patients undergoing successful pancreas transplantation have normal glucose levels in the fasting and fed states and normal levels of hemoglobin A(1c) without use of exogenous insulin or any other medications for diabetes. In some of these patients, these measures have remained stable for more than 10 years. Additionally pancreas transplant recipients recover from short-term hypoglycemia produced by an intravenous pulse of insulin. However, metabolic success has been determined by relatively routine, unsophisticated tests such as oral and intravenous glucose tolerance tests or stimulation with intravenous arginine. These tests may not provide measures of the functional reserve of the pancreas, which is called on during periods of maximal stress. Consequently, we designed studies to ascertain beta and alpha cell performance in recipients of whole pancreas transplants and recipients of a segment of a living related donor. All recipients were recruited from the University of Minnesota Transplant Registry, Minneapolis, Minnesota. Successfully transplated recipients were subjected to prolonged hyperglycemia to assess insulin secretory reserve using the method of glucose potentiation of arginine induced insulin secretion and to prolonged hypoglycemia to assess glucagon responsiveness and hepatic glucose production using the techique of the hyperinsulinemic hypoglycemic clamp. Our studies show that pancreas transplant recipients have markedly diminished insulin secretory reserve, a defect not evident with conventional tests of beta-cell function. No difference was found between the whole graft and segmental recipients. Pancreas transplantation restores the defective glucagon secretory response and enhances hepatic glucose production during prolonged hypoglycemia in subjects with type I diabetes. We conclude that pancreas transplantation does not completely restore beta-cell secretory reserve. This defect might be probably caused in part by cyclosporine and by the procedure involved in transplanting a cadaveric pancreas. Pancreas transplantation normalizes hypoglycemia-induced glucagon secretion and hepatic glucose production, thereby allowing for normalization of glucose recovery from hypoglycemia.

Translated title of the contributionPancreas transplant function in humans undergoing metabolic stress
Original languageGerman
Pages (from-to)188-192
Number of pages5
JournalSwiss Surgery
Issue number4
StatePublished - 1995
Externally publishedYes


  • cyclosporine
  • glucagon
  • glucoc orticoids
  • immunosuppression
  • insulin
  • transplantation


Dive into the research topics of 'Pancreas transplant function in humans undergoing metabolic stress'. Together they form a unique fingerprint.

Cite this