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Sequential Metabolic Studies of Pancreas Allograft Function in Type 1 Diabetic Recipients
Author(s) -
Cottrell Daryl A.,
Henry Mitchell L.,
O'Dorisio Thomas M.,
Tesi Raymond J.,
Ferguson Ronald M.,
Osei Kwame
Publication year - 1992
Publication title -
diabetic medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.474
H-Index - 145
eISSN - 1464-5491
pISSN - 0742-3071
DOI - 10.1111/j.1464-5491.1992.tb01814.x
Subject(s) - medicine , pancreas transplantation , pancreas , type 1 diabetes , artificial pancreas , diabetes mellitus , endocrinology , transplantation , kidney transplantation
We have previously shown that the loss of acute first phase insulin secretion precedes pancreas allograft rejection and development of glucose intolerance in Type 1 diabetic patients. In order to examine whether there is a progressive loss of phases of insulin secretion and beta‐cell function in technically successful pancreas transplants during the first year, we measured glucose, insulin, and C‐peptide responses to physiological (mixed meal) and pharmacological (IV glucose and IV glucagon) stimulation in 27 glucose‐tolerant, insulin‐independent allograft recipients at 3, 6, and 12 months. Mean ± SE fasting serum glucose levels were normalized throughout the study period. Postprandial serum glucose profiles tended to increase by 12 months compared to 3 and 6 months, although peak glucose levels were not statistically different. Following pancreas transplantation, basal serum insulin levels were high at 3 months (163 ± 17 pM), 6 months (165 ± 22 pM), and 12 months (248 ± 54 pM, p = NS) in the Type 1 diabetic pancreas allograft recipients when compared to normal (25 ± 3 pM). We observed slight elevations in postprandial insulin and C‐peptide profiles at 12 months compared to 3 and 6 months. Following IV glucose and glucagon stimulation, serum insulin and C‐peptide levels as well as phases of insulin release did not differ over the 12‐month study period. Similarly, the glucose decay constant ( K G ) was nearly identical at 3, 6, and 12 months. In summary, 1 year following successful whole cadaveric, heterotopic pancreas transplantation in Type 1 diabetic recipients, fasting serum glucose remains normalized, while postprandial glucose tends to rise. This alteration in post‐mixed meal glucose tolerance is achieved at the expense of elevated basal and post‐stimulation insulin and C‐peptide levels, suggesting worsening of the insulin‐resistant state in such patients. The upward trend in glucose levels was observed only after mixed meal but not intravenous glucose stimulation. In addition, the acute first and second phase insulin release to both glucose and non‐glucose stimuli, which are more sensitive markers for beta‐cell dysfunction, were preserved 12 months following pancreas transplantation in Type 1 diabetic recipients.