ArticleEndocrinology2010
Cholecystokinin is up-regulated in obese mouse islets and expands beta-cell mass by increasing beta-cell survival.
Article in Endocrinology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 69 citations in OpenAlex.
- Disentangling batch effects and biological signals across conditions in single-cell transcriptome.Patterns (New York, N.Y.) · 2026Article
- Beta cell-derived cholecystokinin drives obesity-associated pancreatic adenocarcinoma development.Nature communications · 2026Article
- Cholecystokinin: Clinical aspects of the new biology.Journal of internal medicine · 2025Review
- The role of gut-islet axis in pancreatic islet function and glucose homeostasis.Diabetes, obesity & metabolism · 2025Review
- Efficacy evaluation and mechanistic investigation of transcutaneous auricular vagus nerve stimulation in enhancing the therapeutic effects of semaglutide and reducing its gastrointestinal side effects: a randomized controlled trial protocol.Frontiers in neurology · 2025Article
- Novel Pharmaceuticals in Appetite Regulation: Exploring emerging gut peptides and their pharmacological prospects.Pharmacology research & perspectives · 2024Review
- Article
- Decoding the obesity-cancer connection: lessons from preclinical models of pancreatic adenocarcinoma.Life science alliance · 2023Review
- The Role of Catechins in Regulating Diabetes: An Update Review.Nutrients · 2022Review
- Cholecystokinin attenuates β-cell apoptosis in both mouse and human islets.Translational research : the journal of laboratory and clinical medicine · 2022Article
- Potential Therapeutic Targeting Neurotransmitter Receptors in Diabetes.Frontiers in endocrinology · 2022Review
- Vaccination with Polyclonal Antibody Stimulator (PAS) Prevents Pancreatic Carcinogenesis in the KRAS Mouse Model.Cancer prevention research (Philadelphia, Pa.) · 2021Article
- Role of Enteroendocrine Hormones in Appetite and Glycemia.Obesity medicine · 2021Article
- Review
- Benefits of Sustained Upregulated Unimolecular GLP-1 and CCK Receptor Signalling in Obesity-Diabetes.Frontiers in endocrinology · 2021Article
- Zonation of Pancreatic Acinar Cells in Diabetic Mice.Cell reports · 2020Article
- Article
- Gastrin, Cholecystokinin, Signaling, and Biological Activities in Cellular Processes.Frontiers in endocrinology · 2020Review
- A gene expression network analysis of the pancreatic islets from lean and obese mice identifies complement 1q like-3 secreted protein as a regulator of β-cell function.Scientific reports · 2019Article
- Premises for Cholecystokinin and Gastrin Peptides in Diabetes Therapy.Clinical medicine insights. Endocrinology and diabetes · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 4 institutions in 1 country.
Funding
Abstract
An absolute or functional deficit in beta-cell mass is a key factor in the pathogenesis of diabetes. We model obesity-driven beta-cell mass expansion by studying the diabetes-resistant C57BL/6-Leptin(ob/ob) mouse. We previously reported that cholecystokinin (Cck) was the most up-regulated gene in obese pancreatic islets. We now show that islet cholecystokinin (CCK) is up-regulated 500-fold by obesity and expressed in both alpha- and beta-cells. We bred a null Cck allele into the C57BL/6-Leptin(ob/ob) background and investigated beta-cell mass and metabolic parameters of Cck-deficient obese mice. Loss of CCK resulted in decreased islet size and reduced beta-cell mass through increased beta-cell death. CCK deficiency and decreased beta-cell mass exacerbated fasting hyperglycemia and reduced hyperinsulinemia. We further investigated whether CCK can directly affect beta-cell death in cell culture and isolated islets. CCK was able to directly reduce cytokine- and endoplasmic reticulum stress-induced cell death. In summary, CCK is up-regulated by islet cells during obesity and functions as a paracrine or autocrine factor to increase beta-cell survival and expand beta-cell mass to compensate for obesity-induced insulin resistance.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.