ArticleAmerican journal of physiology. Endocrinology and metabolism2015
Cholecystokinin expression in the β-cell leads to increased β-cell area in aged mice and protects from streptozotocin-induced diabetes and apoptosis.
Article in American journal of physiology. Endocrinology and metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 45 citations in OpenAlex.
- Beta cell-derived cholecystokinin drives obesity-associated pancreatic adenocarcinoma development.Nature communications · 2026Article
- CCK-1R-selective and non-selective cholecystokinin antagonists, lorglumide, and proglumide increased toxicity of carboplatin to granulocyte-macrophage progenitor cells (CFU-GM) of bone marrow of rats.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Article
- Cholecystokinin: Clinical aspects of the new biology.Journal of internal medicine · 2025Review
- Article
- A Supportive Role of Mesenchymal Stem Cells on Insulin-Producing Langerhans Islets with a Specific Emphasis on The Secretome.Biomedicines · 2023Review
- Verapamil chronicles: advances from cardiovascular to pancreatic β-cell protection.Frontiers in pharmacology · 2023Review
- Transgenic overexpression of microRNA-30d in pancreatic beta-cells progressively regulates beta-cell function and identity.Scientific reports · 2022Article
- 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
- Pancreatic β cell-selective zinc transporter 8 insufficiency accelerates diabetes associated with islet amyloidosis.JCI insight · 2021Article
- microRNA-483 Protects Pancreatic β-Cells by Targeting ALDH1A3.Endocrinology · 2021Article
- Benefits of Sustained Upregulated Unimolecular GLP-1 and CCK Receptor Signalling in Obesity-Diabetes.Frontiers in endocrinology · 2021Article
- Article
- Intra-islet GLP-1, but not CCK, is necessary for β-cell function in mouse and human islets.Scientific reports · 2020Article
- Gastrin, Cholecystokinin, Signaling, and Biological Activities in Cellular Processes.Frontiers in endocrinology · 2020Review
- Trim33 (Tif1γ) is not required for skeletal muscle development or regeneration but suppresses cholecystokinin expression.Scientific reports · 2019Article
- 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
- Is There a Role for Bioactive Lipids in the Pathobiology of Diabetes Mellitus?Frontiers in endocrinology · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Cholecystokinin (CCK) is a peptide hormone produced in the gut and brain with beneficial effects on digestion, satiety, and insulin secretion. CCK is also expressed in pancreatic β-cells, but only in models of obesity and insulin resistance. Whole body deletion of CCK in obese mice leads to reduced β-cell mass expansion and increased apoptosis. We hypothesized that islet-derived CCK is important in protection from β-cell apoptosis. To determine the specific role of β-cell-derived CCK in β-cell mass dynamics, we generated a transgenic mouse that expresses CCK in the β-cell in the lean state (MIP-CCK). Although this transgene contains the human growth hormone minigene, we saw no expression of human growth hormone protein in transgenic islets. We examined the ability of MIP-CCK mice to maintain β-cell mass when subjected to apoptotic stress, with advanced age, and after streptozotocin treatment. Aged MIP-CCK mice have increased β-cell area. MIP-CCK mice are resistant to streptozotocin-induced diabetes and exhibit reduced β-cell apoptosis. Directed CCK overexpression in cultured β-cells also protects from cytokine-induced apoptosis. We have identified an important new paracrine/autocrine effect of CCK in protection of β-cells from apoptotic stress. Understanding the role of β-cell CCK adds to the emerging knowledge of classic gut peptides in intraislet signaling. CCK receptor agonists are being investigated as therapeutics for obesity and diabetes. While these agonists clearly have beneficial effects on body weight and insulin sensitivity in peripheral tissues, they may also directly protect β-cells from apoptosis.
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.