Increased proliferation of the pancreatic duct gland compartment in type 1 diabetes
The Journal of Clinical Endocrinology & Metabolism, 2017•academic.oup.com
Abstract Context: Pancreatic duct glands (PDGs) have been proposed as a source of
regeneration in response to exocrine pancreas injury, and thus may serve as an organ stem
cell niche. There is evidence to suggest ongoing β-cell formation in longstanding type 1
diabetes (T1D), but the source is unknown. Objective: To investigate the PDG compartment
of the pancreas in humans with T1D for evidence of an active regenerative signature
(presence of progenitor cells and increased proliferation) and, in particular, as a potential …
regeneration in response to exocrine pancreas injury, and thus may serve as an organ stem
cell niche. There is evidence to suggest ongoing β-cell formation in longstanding type 1
diabetes (T1D), but the source is unknown. Objective: To investigate the PDG compartment
of the pancreas in humans with T1D for evidence of an active regenerative signature
(presence of progenitor cells and increased proliferation) and, in particular, as a potential …
Context
Pancreatic duct glands (PDGs) have been proposed as a source of regeneration in response to exocrine pancreas injury, and thus may serve as an organ stem cell niche. There is evidence to suggest ongoing β-cell formation in longstanding type 1 diabetes (T1D), but the source is unknown.
Objective
To investigate the PDG compartment of the pancreas in humans with T1D for evidence of an active regenerative signature (presence of progenitor cells and increased proliferation) and, in particular, as a potential source of β-cells.
Design, Setting, and Participants
Pancreases from 46 brain dead organ donors (22 with T1D, 24 nondiabetic controls) were investigated for activation (increased proliferation) and markers of pancreatic exocrine and endocrine progenitors.
Results
PDG cell replication was increased in T1D (6.3% ± 1.6% vs 0.6% ± 0.1%, P < 0.001, T1D vs nondiabetic), most prominently in association with pancreatic inflammation. There were increased progenitor-like cells in PDGs of T1D, but predominantly with an exocrine fate.
Conclusion
The PDG compartment is activated in T1D consistent with a response to ongoing inflammation, and via resulting ductal hyperplasia may contribute to local obstructive pancreatitis and eventual pancreatic atrophy characteristic of T1D. However, there is no evidence of effective endocrine cell formation from PDGs.
Oxford University Press