AJP - Endocrinology and Metabolism, Vol 261, Issue 6 E800-E808, Copyright © 1991 by American Physiological Society
Islet cell responses to glucose in human transplanted pancreas
D. Elahi, B. A. Clark, M. McAloon-Dyke, G. Wong, R. Brown, M. Shapiro, K. L. Minaker, T. L. Flanagan, T. Pruett, R. Gingerich and al. et
Division on Aging, Harvard Medical School, Charles A. Dana Research Institute, Boston, Massachusetts.
Postsurgery, pancreas transplantation results in alterations of
carbohydrate metabolism. Additionally, immunosuppressive therapy impacts on
glucose regulation. We evaluated the hormonal and metabolic responses of
pancreas allografts, utilizing the hyperglycemic clamp technique coupled
with the tritiated glucose methodology, in 11 volunteers who had received
simultaneous pancreas-kidney transplantation (P-K) with systemic drainage.
Their responses were compared with seven volunteers who had received only a
kidney (K) graft and with seven normal control (C) volunteers. Although
basal glucose and hepatic glucose output were similar in all three groups,
basal insulin, C-peptide, glucagon, and pancreatic polypeptide were highest
in the P-K group and lowest in normal subjects. During hyperglycemia, all
groups showed a similar characteristic, initial complete suppression of
hepatic glucose production, with recovery followed by a later suppression.
Peripheral glucose uptake was similar in P-K and C subjects but decreased
in K patients. Systemic insulin levels were fourfold higher in the pancreas
transplant patients than in healthy subjects. Thus, under basal and
hyperglycemic stimulation, 1) hepatic glucose homeostasis is regulated
normally, even with pancreatic drainage into the systemic circulation; 2)
overall glucose disposal is normal in P-K patients because of marked
hyperinsulinemia; and 3) there is loss of tonic inhibition of endocrine
pancreatic function secondary to pancreatic denervation.
