Exp Clin Endocrinol Diabetes 2007; 115(10): 647-653
DOI: 10.1055/s-2007-982501
Article

© J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York

Impaired Glucose Tolerance in Pancreas Grafted Diabetic Patients is Due to Insulin Secretory Defects

C. D. Dieterle 1 , M. Veitenhansl 1 , B. Gutt 1 , H. Arbogast 2 , G. R. Meier 1 , W.-D. Illner 2 , A. Schlamp 1 , J. Seissler 1 , R. Landgraf 1
  • 1Diabetes Centre, Medizinische Klinik Innenstadt
  • 2Division of Transplant Surgery, Grosshadern, Klinikum University of Munich, Germany
Further Information

Publication History

received 13.12.2006 first decision 01.05.2007

accepted 23.05.2007

Publication Date:
30 November 2007 (online)

Abstract

Introduction: Pancreas transplantation in diabetic patients can sustain insulin independence for years. The aim of the study was to measure the incidence of an impaired or diabetic glucose tolerance in patients after successful transplantation and analyse insulin resistance and insulin secretion.

Methods: 174 Type 1 diabetic recipients of simultaneous pancreas/kidney (SPK) transplants were investigated early (three months) and 95 patients late (five years) after transplantation using an oral glucose tolerance test combined with an iv arginine load.

Results: Although mean fasting blood glucose and HbA1c levels were within the normal range, only 65% of the patients displayed a normal glucose tolerance (NGT), whereas 25% had an impaired (IGT) and 10% showed a diabetic glucose tolerance (DGT). Fasting blood glucose and HbA1c values were significantly lower in patients with NGT compared to graft recipients with IGT or DGT, either three months or five years after SPK. Indicators of insulin resistance (fasting insulin, HOMA-IR, Matsuda/de Fronzo Index) were elevated in all graft recipients, but no differences were found between groups. In contrast insulin secretion was significantly reduced in patients with IGT and DGT early and late after transplantation.

Summary: Insulin resistance is a common feature after pancreas transplantation. However, either three months or five years after SPK abnormal glucose tolerance was mainly due to a reduced glucose- and arginine-induced secretory response of insulin.

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Correspondence

Dr. C. D. Dieterle

Diabetes Center

Medizinische Klinik

Ziemssenstr.1

80336 München

Germany

Phone: +49/89/5160 23 63

Fax: +49/89/5160 29 68

Email: christoph.dieterle@med.uni-muenchen.de

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