ArticleScientific reports2024
Cystic fibrosis-related diabetes is associated with reduced islet protein expression of GLP-1 receptor and perturbation of cell-specific transcriptional programs.
Article in Scientific reports, 2024. 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.
- Unravelling the developmental origins of cystic fibrosis-related diabetes.Diabetologia · 2026Review
- Glucagon-Like Peptide-1 Receptor Agonists: Their Therapeutic Potential in Cystic Fibrosis.Advances in therapy · 2026Review
- The endocrine complications of cystic fibrosis.Nature reviews. Endocrinology · 2026Review
- Approach to the Patient With Pancreatogenic Diabetes.The Journal of clinical endocrinology and metabolism · 2026Review
- Elexacaftor-tezacaftor-ivacaftor enhances first-phase insulin secretion and improves glucose control in cystic fibrosis.Endocrine connections · 2026Article
- Glucagon-like peptide-1 receptor agonists in adults with cystic fibrosis-related diabetes: Rationale and emerging evidence.Diabetes, obesity & metabolism · 2025Article
- Localized GLP1 receptor pre-internalization directs pancreatic alpha cell to beta cell communication.Cell metabolism · 2025Article
- How Effectively Can Oxidative Stress and Inflammation Be Reversed When CFTR Function Is Pharmacologically Improved?Antioxidants (Basel, Switzerland) · 2025Review
- Pancreas and islet morphology in cystic fibrosis: clues to the etiology of cystic fibrosis-related diabetes.Frontiers in endocrinology · 2023Review
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Authors and funding
8 authors.
Funding
Abstract
Insulin secretion is impaired in individuals with cystic fibrosis (CF), contributing to high rates of CF-related diabetes (CFRD) and substantially increasing disease burden. To develop improved therapies for CFRD, better knowledge of pancreatic pathology in CF is needed. Glucagon like peptide-1 (GLP-1) from islet α cells potentiates insulin secretion by binding GLP-1 receptors (GLP-1Rs) on β cells. We determined whether expression of GLP-1 and/or its signaling components are reduced in CFRD, thereby contributing to impaired insulin secretion. Immunohistochemistry of pancreas from humans with CFRD versus no-CF/no-diabetes revealed no difference in GLP-1 immunoreactivity per islet area, whereas GLP-1R immunoreactivity per islet area or per insulin-positive islet area was reduced in CFRD. Using spatial transcriptomics, we observed several differentially expressed α- and/or β-cell genes between CFRD and control pancreas. In CFRD, we found upregulation of α-cell PCSK1 which encodes the enzyme (PC1/3) that generates GLP-1, and downregulation of α-cell PCSK1N which inhibits PC1/3. Gene set enrichment analysis also revealed α and β cell-specific pathway dysregulation in CFRD. Together, our data suggest intra-islet GLP-1 is not limiting in CFRD, but its action may be restricted due to reduced GLP-1R protein levels. Thus, restoring β-cell GLP-1R protein expression may improve β-cell function in CFRD.
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