ArticleMolecular endocrinology (Baltimore, Md.)2015
Glucagon-Like Peptide-1 Regulates Cholecystokinin Production in β-Cells to Protect From Apoptosis.
Article in Molecular endocrinology (Baltimore, Md.), 2015. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- Efficacy and Safety of Glucagon-Like Peptide-1 Receptor Agonists Following Bariatric Surgery: A Systematic Review and Meta-Analysis.Endocrinology, diabetes & metabolism · 2026Pooled it
- Beta cell-derived cholecystokinin drives obesity-associated pancreatic adenocarcinoma development.Nature communications · 2026Article
- Article
- Cholecystokinin: Clinical aspects of the new biology.Journal of internal medicine · 2025Review
- Use of GLP-1 Receptor Agonists for the Management of Type 1 Diabetes: A Pediatric Perspective.Hormone research in paediatrics · 2025Review
- Article
- A Supportive Role of Mesenchymal Stem Cells on Insulin-Producing Langerhans Islets with a Specific Emphasis on The Secretome.Biomedicines · 2023Review
- Cholecystokinin attenuates β-cell apoptosis in both mouse and human islets.Translational research : the journal of laboratory and clinical medicine · 2022Article
- Positive Interventional Effect of Engineered Butyrate-Producing Bacteria on Metabolic Disorders and Intestinal Flora Disruption in Obese Mice.Microbiology spectrum · 2022Article
- Exenatide exerts a neuroprotective effect against diabetic cognitive impairment in rats by inhibiting apoptosis: Role of the JNK/c‑JUN signaling pathway.Molecular medicine reports · 2022Article
- Pharmacological blockade of the EP3 prostaglandin EMolecular metabolism · 2021Article
- Role of Enteroendocrine Hormones in Appetite and Glycemia.Obesity medicine · 2021Article
- Current and future therapies for type 1 diabetes.Diabetologia · 2021Review
- Harnessing the Endogenous Plasticity of Pancreatic Islets: A Feasible Regenerative Medicine Therapy for Diabetes?International journal of molecular sciences · 2021Review
- Review
- Benefits of Sustained Upregulated Unimolecular GLP-1 and CCK Receptor Signalling in Obesity-Diabetes.Frontiers in endocrinology · 2021Article
- Updating the Role of α-Cell Preproglucagon Products on GLP-1 Receptor-Mediated Insulin Secretion.Diabetes · 2020Article
- Regenerative medicine of pancreatic islets.World journal of gastroenterology · 2020Review
- Article
- Glucagon-Like Peptide-1: Actions and Influence on Pancreatic Hormone Function.Comprehensive Physiology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Cholecystokinin (CCK) is a classic gut hormone that is also expressed in the pancreatic islet, where it is highly up-regulated with obesity. Loss of CCK results in increased β-cell apoptosis in obese mice. Similarly, islet α-cells produce increased amounts of another gut peptide, glucagon-like peptide 1 (GLP-1), in response to cytokine and nutrient stimulation. GLP-1 also protects β-cells from apoptosis via cAMP-mediated mechanisms. Therefore, we hypothesized that the activation of islet-derived CCK and GLP-1 may be linked. We show here that both human and mouse islets secrete active GLP-1 as a function of body mass index/obesity. Furthermore, GLP-1 can rapidly stimulate β-cell CCK production and secretion through direct targeting by the cAMP-modulated transcription factor, cAMP response element binding protein (CREB). We find that cAMP-mediated signaling is required for Cck expression, but CCK regulation by cAMP does not require stimulatory levels of glucose or insulin secretion. We also show that CREB directly targets the Cck promoter in islets from obese (Leptin(ob/ob)) mice. Finally, we demonstrate that the ability of GLP-1 to protect β-cells from cytokine-induced apoptosis is partially dependent on CCK receptor signaling. Taken together, our work suggests that in obesity, active GLP-1 produced in the islet stimulates CCK production and secretion in a paracrine manner via cAMP and CREB. This intraislet incretin loop may be one mechanism whereby GLP-1 protects β-cells from apoptosis.
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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 Socratic graph.