ArticleNature metabolism2022
Abnormal exocrine-endocrine cell cross-talk promotes β-cell dysfunction and loss in MODY8.
Article in Nature metabolism, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- Pooled it
- ProtectiveiScience · 2026Article
- Genetic spectrum and treatment implications of maturity-onset diabetes of the young in the eastern Black Sea region of Türkiye: a combined adult and pediatric cohort of 296 patients with identification of rare and novel variants.Molecular biology reports · 2026Article
- Oncocytic Adrenocortical Carcinoma with Somatic Pathogenic Variants ofDiagnostics (Basel, Switzerland) · 2026Article
- Beta cell-derived cholecystokinin drives obesity-associated pancreatic adenocarcinoma development.Nature communications · 2026Article
- Novel variation in theFrontiers in endocrinology · 2026Review
- Genome-wide CRISPR Screen Identifies Sec31A as a Key Regulator of Alpha Cell Survival.Nature communications · 2025Article
- The Hippo terminal effector YAP boosts enterovirus replication in type 1 diabetes.Nature communications · 2025Article
- Pancreatic exocrine damage induces beta cell stress in zebrafish larvae.Diabetologia · 2025Article
- Vanishing pancreas: CT and MRI features and imaging diagnostic strategies.Insights into imaging · 2025Article
- The MODY-Causing Mutation of the Human Carboxyl Ester Lipase Gene (CEL) Triggers Chronic Pancreatitis But Not Diabetes in Mice.Gastroenterology · 2025Article
- Integrating Spatial and Single-Nucleus Transcriptomic Data to Assess the Effects of Intrauterine Hyperglycemia on Fetal Pancreatic Development.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Rare forms of monogenic diabetes in non-European individuals. First reports of CEL and RFX6 mutations from the Indian subcontinent.Acta diabetologica · 2025Article
- The perfect storm: unraveling the interplay of genetic predisposition and viral triggers in type 1 diabetes pathogenesis.Frontiers in endocrinology · 2025Review
- Pancreatic agenesis and altered m6A methylation in the pancreas of PDX1-mutant cynomolgus macaques.Zoological research · 2024Article
- Examining the liver-pancreas crosstalk reveals a role for the molybdenum cofactor in β-cell regeneration.Life science alliance · 2024Article
- mThe EMBO journal · 2024Article
- Recent progress in modeling and treating diabetes using stem cell-derived islets.Stem cells translational medicine · 2024Review
- Article
- Identification of unique cell type responses in pancreatic islets to stress.Nature communications · 2024Article
Corrections and comments
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Authors and funding
15 authors at 6 institutions in 2 countries.
Funding
Abstract
MODY8 (maturity-onset diabetes of the young, type 8) is a dominantly inherited monogenic form of diabetes associated with mutations in the carboxyl ester lipase (CEL) gene expressed by pancreatic acinar cells. MODY8 patients develop childhood-onset exocrine pancreas dysfunction followed by diabetes during adulthood. However, it is unclear how CEL mutations cause diabetes. In the present study, we report the transfer of CEL proteins from acinar cells to β-cells as a form of cross-talk between exocrine and endocrine cells. Human β-cells show a relatively higher propensity for internalizing the mutant versus the wild-type CEL protein. After internalization, the mutant protein forms stable intracellular aggregates leading to β-cell secretory dysfunction. Analysis of pancreas sections from a MODY8 patient reveals the presence of CEL protein in the few extant β-cells. The present study provides compelling evidence for the mechanism by which a mutant gene expressed specifically in acinar cells promotes dysfunction and loss of β-cells to cause diabetes.
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