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Original Research

Marked Expansion of Exocrine and Endocrine Pancreas With Incretin Therapy in Humans With Increased Exocrine Pancreas Dysplasia and the Potential for Glucagon-Producing Neuroendocrine Tumors

  1. Alexandra E. Butler1⇑,
  2. Martha Campbell-Thompson2,
  3. Tatyana Gurlo1,
  4. David W. Dawson3,
  5. Mark Atkinson2 and
  6. Peter C. Butler1
  1. 1Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California
  2. 2Departments of Pathology and Pediatrics, College of Medicine, University of Florida, Gainesville, Florida.
  3. 3Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California
  1. Corresponding author: Alexandra E. Butler, aebutler{at}mednet.ucla.edu.
Diabetes 2013 Jul; 62(7): 2595-2604. https://doi.org/10.2337/db12-1686
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Abstract

Controversy exists regarding the potential regenerative influences of incretin therapy on pancreatic β-cells versus possible adverse pancreatic proliferative effects. Examination of pancreata from age-matched organ donors with type 2 diabetes mellitus (DM) treated by incretin therapy (n = 8) or other therapy (n = 12) and nondiabetic control subjects (n = 14) reveals an ∼40% increased pancreatic mass in DM treated with incretin therapy, with both increased exocrine cell proliferation (P < 0.0001) and dysplasia (increased pancreatic intraepithelial neoplasia, P < 0.01). Pancreata in DM treated with incretin therapy were notable for α-cell hyperplasia and glucagon-expressing microadenomas (3 of 8) and a neuroendocrine tumor. β-Cell mass was reduced by ∼60% in those with DM, yet a sixfold increase was observed in incretin-treated subjects, although DM persisted. Endocrine cells costaining for insulin and glucagon were increased in DM compared with non-DM control subjects (P < 0.05) and markedly further increased by incretin therapy (P < 0.05). In conclusion, incretin therapy in humans resulted in a marked expansion of the exocrine and endocrine pancreatic compartments, the former being accompanied by increased proliferation and dysplasia and the latter by α-cell hyperplasia with the potential for evolution into neuroendocrine tumors.

Footnotes

  • This article contains Supplementary Data online at http://diabetes.diabetesjournals.org/lookup/suppl/doi:10.2337/db12-1686/-/DC1.

  • See accompanying commentary, p. 2178.

  • Received December 4, 2012.
  • Accepted March 14, 2013.
  • © 2013 by the American Diabetes Association.

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

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Marked Expansion of Exocrine and Endocrine Pancreas With Incretin Therapy in Humans With Increased Exocrine Pancreas Dysplasia and the Potential for Glucagon-Producing Neuroendocrine Tumors
Alexandra E. Butler, Martha Campbell-Thompson, Tatyana Gurlo, David W. Dawson, Mark Atkinson, Peter C. Butler
Diabetes Jul 2013, 62 (7) 2595-2604; DOI: 10.2337/db12-1686

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Marked Expansion of Exocrine and Endocrine Pancreas With Incretin Therapy in Humans With Increased Exocrine Pancreas Dysplasia and the Potential for Glucagon-Producing Neuroendocrine Tumors
Alexandra E. Butler, Martha Campbell-Thompson, Tatyana Gurlo, David W. Dawson, Mark Atkinson, Peter C. Butler
Diabetes Jul 2013, 62 (7) 2595-2604; DOI: 10.2337/db12-1686
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