ArticleEuropean journal of clinical investigation2025
Incretin system and glucagon secretion in patients with chronic pancreatitis.
Article in European journal of clinical investigation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Glucose-lowering therapy in diabetes of the exocrine pancreas: a real-world evidence analysis in a tertiary hospital in the timeframe 2018-2022.Therapeutic advances in endocrinology and metabolism · 2026Article
- Incretin system and glucagon secretion in patients with chronic pancreatitis.European journal of clinical investigation · 2025Article
- Use of hybrid closed-loop insulin pump in pancreatogenic diabetes following necrotizing hemorrhagic pancreatitis: a case report.Frontiers in clinical diabetes and healthcare · 2025Article
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Authors and funding
17 authors.
Funding
Abstract
backgroundDiabetes of the exocrine pancreas (DEP) is an underdiagnosed form of diabetes, prevalently caused by acute and chronic pancreatitis (CP). The contribution of incretin system dysfunction and the role of glucagon levels in the pathogenesis of DEP remain unclear. The aim of our study is to assess the secretion of glucagon like peptide-1 (GLP-1), glucose-dependent insulinotropic peptide (GIP) and glucagon, along with the incretin effect, in individuals with and without CP. By comparing these parameters within the same glucose tolerance class, we seek to elucidate specific hormonal alterations that characterize DEP.
methodsTo pursue this aim, we conducted a cross-sectional study on 32 patients with chronic pancreatitis (wCP) and 60 patients without chronic pancreatitis (w/oCP), who were administered an oral glucose tolerance test, a hyperglycemic clamp and a mixed meal test with measurement of glucose, insulin, C-peptide, GLP-1, GIP and glucagon.
resultsThe comparison between individuals wCP and w/oCP showed worse beta-cell function and lower incretin effect for the former, but incretin and glucagon levels were similar. Diabetes prevalence was higher in the group wCP than in the group w/oCP (56% vs. 33%). Thus, to evaluate the differences determined by CP, we found it necessary to stratify individuals according to glucose tolerance class. After stratification, we found that both groups had similar beta-cell function, incretin effect and incretin and glucagon secretion.
conclusionsTherefore, incretin and glucagon levels and the incretin effect varied according to glucose tolerance, not the presence or absence of CP. Similar defects in incretin secretion and effects are responsible for diabetes development in individuals wCP and w/oCP.
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