ArticleDiabetologia2009
Pancreatic adenocarcinoma patients with localised chronic severe pancreatitis show an increased number of single beta cells, without alterations in fractional insulin area.
Article in Diabetologia, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- Activated pancreatic stellate cells can impair pancreatic islet function in mice.Upsala journal of medical sciences · 2015Article
- New insight on human type 1 diabetes biology: nPOD and nPOD-transplantation.Current diabetes reports · 2014Review
- The diagnosis of insulitis in human type 1 diabetes.Diabetologia · 2013Article
- Network for Pancreatic Organ Donors with Diabetes (nPOD): developing a tissue biobank for type 1 diabetes.Diabetes/metabolism research and reviews · 2012Review
- Staining protocols for human pancreatic islets.Journal of visualized experiments : JoVE · 2012Article
- Enhanced expression of Pctk1, Tcf12 and Ccnd1 in hippocampus of rats: Impact on cognitive function, synaptic plasticity and pathology.Neurobiology of learning and memory · 2012Article
- Article
- Evidence of increased islet cell proliferation in patients with recent-onset type 1 diabetes.Diabetologia · 2010Article
- Histopathology of type 1 diabetes: old paradigms and new insights.The review of diabetic studies : RDS · 2009Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
aims/hypothesisRecent histological analysis of pancreases obtained from patients with long-standing type 1 diabetes identified chronic islet inflammation and limited evidence suggestive of beta cell replication. Studies in rodent models also suggest that beta cell replication can be induced by certain inflammatory cytokines and by gastrin. We therefore tested the hypothesis that beta cell replication is observed in non-autoimmune human pancreatic disorders in which localised inflammation or elevated gastrin levels are present.
methodsResected operative pancreatic specimens were obtained from patients diagnosed with primary adenocarcinoma (with or without chronic severe pancreatitis) or gastrinoma. Additional pancreatic tissue was obtained from autopsy control patients. Immunohistochemistry was used to assess fractional insulin area, beta cell number and replication rate and differentiation factors relevant to beta cell development.
resultsFractional insulin area was similar among groups. Patients with pancreatic adenocarcinoma and localised chronic severe pancreatitis displayed significant increases in the number of single beta cells, as well as increased beta cell replication rate and levels of neurogenic differentiation 1 in islets. Patients with gastrinoma demonstrated significant increases in the number of single beta cells, but the beta cell replication rate and islet differentiation factor levels were similar to those in the control group. CONCLUSIONS/
interpretationThese findings indicate that chronic severe pancreatic inflammation can be associated with significant effects on beta cell number or replication rate, depending on the distribution of the cells. This information may prove useful for attempts seeking to design therapies aimed at inducing beta cell replication as a means of reversing diabetes.
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