ArticleDiabetes2014
Carboxyl-ester lipase maturity-onset diabetes of the young is associated with development of pancreatic cysts and upregulated MAPK signaling in secretin-stimulated duodenal fluid.
Article in Diabetes, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses that pooled it.
What it found
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The trial behind it
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Who cites it
25 citing papers in PubMed, 2 syntheses or guidelines pooled it, 44 citations in OpenAlex.
- Treatment Options for Patients with Maturity-Onset Diabetes of the Young (MODY): A Systematic Review of Literature: 2026 Update.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2026Pooled it
- Pooled it
- Exocrine Pancreatic Insufficiency Manifesting Before Insulin Dependence in Adult-Onset Type 1 Diabetes.Clinical case reports · 2026Article
- Unraveling the genetic basis of MODY: insights from next-generation sequencing.Journal of applied genetics · 2025Article
- Common single-base insertions in the VNTR of the carboxyl ester lipase (CEL) gene are benign and also likely to arise somatically in the exocrine pancreas.Human molecular genetics · 2024Article
- Excess pancreatic elastase alters acinar-β cell communication by impairing the mechano-signaling and the PAR2 pathways.Cell metabolism · 2023Article
- ISPAD Clinical Practice Consensus Guidelines 2022: The diagnosis and management of monogenic diabetes in children and adolescents.Pediatric diabetes · 2022Article
- Endoplasmic stress-inducing variants in carboxyl ester lipase and pancreatic cancer risk.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2022Article
- Maturity-Onset Diabetes of the Young: Mutations, Physiological Consequences, and Treatment Options.Journal of personalized medicine · 2022Review
- Spatial Environment Affects HNF4A Mutation-Specific Proteome Signatures and Cellular Morphology in hiPSC-Derived β-Like Cells.Diabetes · 2022Article
- Two New Mutations in the CEL Gene Causing Diabetes and Hereditary Pancreatitis: How to Correctly Identify MODY8 Cases.The Journal of clinical endocrinology and metabolism · 2022Article
- Abnormal exocrine-endocrine cell cross-talk promotes β-cell dysfunction and loss in MODY8.Nature metabolism · 2022Article
- 100 YEARS OF INSULIN: A brief history of diabetes genetics: insights for pancreatic beta-cell development and function.The Journal of endocrinology · 2021Review
- Discovery of New Protein Targets of BPA Analogs and Derivatives Associated with Noncommunicable Diseases: A Virtual High-Throughput Screening.Environmental health perspectives · 2021Article
- Single nucleotide polymorphisms in CEL-HYB1 increase risk for chronic pancreatitis through proteotoxic misfolding.Human mutation · 2020Article
- A tale of two pancreases: exocrine pathology and endocrine dysfunction.Diabetologia · 2020Review
- HNF4A and GATA6 Loss Reveals Therapeutically Actionable Subtypes in Pancreatic Cancer.Cell reports · 2020Article
- Pathogenic Carboxyl Ester Lipase (CEL) Variants Interact with the Normal CEL Protein in Pancreatic Cells.Cells · 2020Article
- Identification of key regulators of pancreatic ductal adenocarcinoma using bioinformatics analysis of microarray data.Medicine · 2019Article
- Loss of complex O-glycosylation impairs exocrine pancreatic function and induces MODY8-like diabetes in mice.Experimental & molecular medicine · 2018Article
Corrections and comments
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Authors and funding
18 authors at 6 institutions in 2 countries.
Funding
Abstract
Carboxyl-ester lipase (CEL) maturity-onset diabetes of the young (MODY) is a monogenic form of diabetes and pancreatic exocrine dysfunction due to mutations in the CEL gene encoding CEL. The pathogenic mechanism for diabetes development is unknown. Since CEL is expressed mainly in pancreatic acinar cells, we asked whether we could find structural pancreatic changes in CEL-MODY subjects during the course of diabetes development. Furthermore, we hypothesized that the diseased pancreas releases proteins that are detectable in pancreatic fluid and potentially reflect activation or inactivation of disease-specific pathways. We therefore investigated nondiabetic and diabetic CEL-mutation carriers by pancreatic imaging studies and secretin-stimulated duodenal juice sampling. The secretin-stimulated duodenal juice was studied using cytokine assays, mass spectrometry (MS) proteomics, and multiplexed MS-based measurement of kinase activities. We identified multiple pancreatic cysts in all eight diabetic mutation carriers but not in any of the four nondiabetic mutation carriers or the six healthy controls. Furthermore, we identified upregulated mitogen-activated protein kinase (MAPK) target proteins and MAPK-driven cytokines and increased MAPK activity in the secretin-stimulated duodenal juice. These findings show that subjects with CEL-MODY develop multiple pancreatic cysts by the time they develop diabetes and that upregulated MAPK signaling in the pancreatic secretome may reflect the pathophysiological development of pancreatic cysts and diabetes.
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Registered trials
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