期刊
DIABETES
卷 62, 期 7, 页码 2595-2604出版社
AMER DIABETES ASSOC
DOI: 10.2337/db12-1686
关键词
-
资金
- nPOD, a collaborative type 1 diabetes research project
- JDRF
- National Institute of Diabetes and Digestive and Kidney Diseases [DK-059579, DK-061539, DK-077967]
- Larry L. Hillblom Foundation
- Peter and Valerie Kompaniez Foundation
Controversy exists regarding the potential regenerative influences of incretin therapy on pancreatic beta-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 similar to 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 alpha-cell hyperplasia and glucagon-expressing microadenomas (3 of 8) and a neuroendocrine tumor. beta-Cell mass was reduced by similar to 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 alpha-cell hyperplasia with the potential for evolution into neuroendocrine tumors.
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