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Comparison of Pancreas-Transplanted Type 1 Diabetic Patients with Portal-Venous Versus Systemic-Venous Graft Drainage: Impact on Glucose Regulatory Hormones and the Growth Hormone/Insulin–Like Growth Factor-I Axis

Medical Research Laboratories (J.F.), Clinical Institute and Medical Department M, Aarhus University Hospital, DK-8000 Aarhus, Denmark; Departments of Medicine (R.A.R., J.M., W.S., M.A.N.) and Surgery (M.B., R.L., J.K.), Ruhr-University, Knappschafts-Krankenhaus, 44780 Bochum, Germany; Department of Internal Medicine I (R.A.R.), University of Heidelberg, 69120 Heidelberg, Germany; Department of Visceral and Transplant Surgery (R.L., J.K.), Medizinische Hochschule Hannover, 30625 Hannover, Germany; and Diabeteszentrum Bad Lauterberg (M.A.N.), 37431 Bad Lauterberg im Harz, Germany

Address all correspondence and requests for reprints to: Dr. Jan Frystyk, Medical Research Laboratories, Aarhus University Hospital, Nørrebrogade 44, DK-8000 Aarhus C, Denmark. E-mail: jan{at}frystyk.dk.

Context: Pancreas grafts can be drained through the iliac vein (systemic drainage) or the portal vein.

Objective: We hypothesized that normalization of portal insulin in patients with portal pancreas graft drainage stimulates the GH/IGF-I axis and thereby contributes to glucose control.

Methods: We compared patients after combined kidney and pancreas transplantation with portal drainage (n = 7) to patients with systemic drainage of the pancreas graft (n = 8) and nondiabetic controls (n = 8). Overnight fasting sera were analyzed for free and total IGF-I and IGF-binding proteins. Glucose regulatory hormones were examined after an oral glucose tolerance test and GH after stimulation with GHRH.

Results: Systemic drainage led to higher basal and stimulated insulin levels than portal drainage (P < 0.05), but increments in response to oral glucose were reduced in both transplanted groups (P < 0.05 vs. controls). However, glucose tolerance was similar in all groups. Circulating free and total IGF-I and IGF-binding protein-3 were similar to control levels in the systemic drainage group but elevated in the portal drainage group (P < 0.05). Consistently, the GH response was reduced in the portal drainage group (P < 0.05 vs. controls) and correlated inversely with free IGF-I (r = –0.63, P < 0.05).

Conclusion: Portal drainage of pancreatic endocrine secretion in pancreas graft recipients raises IGF-I and lowers GH secretion. These changes might explain that glucose regulation is maintained despite lower peripheral insulin levels, compared with patients with systemic graft drainage and nondiabetic control subjects.