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PARTIAL PANCREATECTOMY IN ADULT HUMANS DOES NOT PROVOKE BETA CELL REGENERATION.

¹: Department of Medicine I, St. Josef-Hospital, Ruhr-University Bochum, Germany
²: Institute for Pathology, Ruhr-University Bochum, Germany
³: Department of Surgery, St. Josef-Hospital, Ruhr-University Bochum, Germany
⁴: Department of Radiology, St. Josef-Hospital, Ruhr-University Bochum, Germany

Introduction: Beta-cell regeneration has been proposed as a possible treatment of diabetes, but the capacity for new beta-cell formation in humans is yet unclear. In young rats partial pancreatectomy prompts new beta cell formation to restore beta cell mass. We addressed the questions: In adult humans: (1) Does partial pancreatectomy provoke new beta-cell formation and increased beta cell mass? (2) Is beta-cell turnover increased after partial pancreatectomy?

Methods: Protocol 1: Human pancreatic tissue was collected from 13 patients who underwent two consecutive partial pancreas resections, and markers of cell turnover were determined in both tissue samples, respectively. Protocol 2: Pancreas volumes were determined from abdominal computer tomography scans, performed in 17 patients on two separate occasions after partial pancreatectomy.

Results: Protocol 1: Fasting glucose concentrations increased significantly after the 50% pancreatectomy (p = 0.01), but fractional beta-cell area of the pancreas remained unchanged (p = 0.11). Beta-cell proliferation, the overall replication index (Ki67 staining), and the percentage of duct cells expressing insulin were similar before and after the partial pancreatectomy. The overall frequency of apoptosis (TUNEL) was slightly increased following the partial pancreatectomy (p = 0.02). Protocol 2: Pancreatic volume was 50% reduced to 35.6 ± 2.6 ccm³ by the partial pancreatectomy. The total pancreatic volume was unchanged after an interval of 247 ± 160 days (35.4 ± 2.7 ccm³; p = 0.51).

Conclusions: Unlike in rodents, a 50 % pancreatectomy does not prompt beta-cell regeneration in adult humans. This explains the high incidence of diabetes after pancreatic resections. Such differences in beta-cell turnover between rodents and humans should be born in mind when evaluating new treatment options aiming to restore beta-cell mass in patients with diabetes.

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