ArticleJCI insight2017
Islet inflammation and ductal proliferation may be linked to increased pancreatitis risk in type 2 diabetes.
Article in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Obesity and diabetes associated with dysregulation of mevalonate pathway markers and progression from pancreatic intraepithelial neoplasia to invasive pancreatic tumor.Stem cell research & therapy · 2026Article
- Bioassay-guided isolation of terpenoids from the soft coralRSC advances · 2025Article
- Exploring the genetic link between gastroesophageal reflux disease and pancreatic cancer: insights from Mendelian randomization.BMC cancer · 2025Article
- Endocrine-exocrine miR-503-322 drives aging-associated pancreatitis via targeting MKNK1 in acinar cells.Nature communications · 2025Article
- Exocrine Pancreas in Type 1 and Type 2 Diabetes: Different Patterns of Fibrosis, Metaplasia, Angiopathy, and Adiposity.Diabetes · 2024Article
- Activation of ductal progenitor-like cells from adult human pancreas requires extracellular matrix protein signaling.iScience · 2024Article
- Testosterone Inhibits Secretion of the Pro-Inflammatory Chemokine CXCL1 from Astrocytes.Current issues in molecular biology · 2024Article
- Exocrine and Endocrine Inflammation Increases Cellular Replication in the Pancreatic Duct Compartment in Type 1 Diabetes.Journal of the Endocrine Society · 2022Article
- Chronic tissue inflammation and metabolic disease.Genes & development · 2021Review
- What can we learn from the islet of Joslin Medalists?Journal of diabetes investigation · 2020Article
- Mesenchymal stem cells ameliorate β cell dysfunction of human type 2 diabetic islets by reversing β cell dedifferentiation.EBioMedicine · 2020Article
- Chronic Pancreatitis and the Development of Pancreatic Cancer.Endocrine, metabolic & immune disorders drug targets · 2020Review
- IAPP toxicity activates HIF1α/PFKFB3 signaling delaying β-cell loss at the expense of β-cell function.Nature communications · 2019Article
- Karyopherin Alpha 2-Expressing Pancreatic Duct Glands and Intra-Islet Ducts in Aged Diabetic C414A-Mutant-CRY1 Transgenic Mice.Journal of diabetes research · 2019Article
- In the setting of β-cell stress, the pancreatic duct gland transcriptome shows characteristics of an activated regenerative response.American journal of physiology. Gastrointestinal and liver physiology · 2018Article
- Increased Chromogranin A-Positive Hormone-Negative Cells in Chronic Pancreatitis.The Journal of clinical endocrinology and metabolism · 2018Article
- Islet α-cell Inflammation Induced By NF-κB inducing kinase (NIK) Leads to Hypoglycemia, Pancreatitis, Growth Retardation, and Postnatal Death in Mice.Theranostics · 2018Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Pancreatitis is more frequent in type 2 diabetes mellitus (T2DM), although the underlying cause is unknown. We tested the hypothesis that ongoing β cell stress and apoptosis in T2DM induces ductal tree proliferation, particularly the pancreatic duct gland (PDG) compartment, and thus potentially obstructs exocrine outflow, a well-established cause of pancreatitis. PDG replication was increased 2-fold in human pancreas from individuals with T2DM, and was associated with increased pancreatic intraepithelial neoplasia (PanIN), lesions associated with pancreatic inflammation and with the potential to obstruct pancreatic outflow. Increased PDG replication in the prediabetic human-IAPP-transgenic (HIP) rat model of T2DM was concordant with increased β cell stress but preceded metabolic derangement. Moreover, the most abundantly expressed chemokines released by the islets in response to β cell stress in T2DM, CXCL1, -4, and -10, induced proliferation in human pancreatic ductal epithelium. Also, the diabetes medications reported as potential modifiers for the risk of pancreatitis in T2DM modulated PDG proliferation accordingly. We conclude that chronic stimulation and proliferation of the PDG compartment in response to islet inflammation in T2DM is a potentially novel mechanism that serves as a link to the increased risk for pancreatitis in T2DM and may potentially be modified by currently available diabetes therapy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.