Evidence map›Paper›PMID 26248680›Full record

ArticleBritish journal of pharmacology2015

Different downstream signalling of CCK1 receptors regulates distinct functions of CCK in pancreatic beta cells.

Shang-lei Ning, Wen-shuai Zheng, Jing Su, Nan Liang, Hui Li, Dao-lai Zhang, Chun-hua Liu, Jun-hong Dong, Zheng-kui Zhang, Min Cui and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
5.9field-weighted citation impact, top 3% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. A Novel CCK Receptor GPR173 Mediates Potentiation of GABAergic Inhibition.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  3. Article
  4. Cholecystokinin attenuates β-cell apoptosis in both mouse and human islets.Translational research : the journal of laboratory and clinical medicine · 2022
    Article
  5. Article
  6. Review
  7. Insects as a New Complex Model in Hormonal Basis of Obesity.International journal of molecular sciences · 2021
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Pancreatic Beta Cell Identity in Humans and the Role of Type 2 Diabetes.Frontiers in cell and developmental biology · 2017
    Review
  19. Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

18 authors at 5 institutions in 1 country.

Shang-lei NingDepartment of Biochemistry and Molecular Biology and Key Laboratory Experimental Teratology of the Ministry of Education, Jinan, Shandong, China.
Wen-shuai ZhengShandong Provincial School Key laboratory for Protein Science of Chronic degenerative diseases, Jinan, Shandong, China.
Jing SuShandong Provincial School Key laboratory for Protein Science of Chronic degenerative diseases, Jinan, Shandong, China.
Nan LiangDepartment of Biochemistry and Molecular Biology and Key Laboratory Experimental Teratology of the Ministry of Education, Jinan, Shandong, China.
Hui LiShandong Provincial School Key laboratory for Protein Science of Chronic degenerative diseases, Jinan, Shandong, China.
Dao-lai ZhangDepartment of Biochemistry and Molecular Biology and Key Laboratory Experimental Teratology of the Ministry of Education, Jinan, Shandong, China.
Chun-hua LiuShandong Provincial School Key laboratory for Protein Science of Chronic degenerative diseases, Jinan, Shandong, China.
Jun-hong DongDepartment of Biochemistry and Molecular Biology and Key Laboratory Experimental Teratology of the Ministry of Education, Jinan, Shandong, China.
Zheng-kui ZhangDepartment of Physiology, Shandong University School of Medicine, Jinan, Shandong, China.
Min CuiDepartment of Physiology, Shandong University School of Medicine, Jinan, Shandong, China.
Qiao-Xia HuDepartment of Biochemistry and Molecular Biology and Key Laboratory Experimental Teratology of the Ministry of Education, Jinan, Shandong, China.
Chao-chao ChenShandong Provincial School Key laboratory for Protein Science of Chronic degenerative diseases, Jinan, Shandong, China.
Chang-hong LiuShandong Provincial Qianfoshan, Shandong University, Jinan, Shandong, China.
Chuan WangDepartment of Pharmacology, Hebei Medical University, Shijiazhuang, Hebei, China.
Qi PangShandong Provincial Hospital, Shandong University, Jinan, Shandong, China.
Yu-xin ChenQilu Hospital, Shandong University, Jinan, Shandong, China.
Xiao YuDepartment of Biochemistry and Molecular Biology and Key Laboratory Experimental Teratology of the Ministry of Education, Jinan, Shandong, China.
Jin-peng SunDepartment of Biochemistry and Molecular Biology and Key Laboratory Experimental Teratology of the Ministry of Education, Jinan, Shandong, China.
Shandong University · CNMinistry of Education of the People's Republic of China · CNHebei Medical University · CNQilu Hospital of Shandong University · CNShandong Provincial Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeCholecystokinin (CCK) is secreted by intestinal I cells and regulates important metabolic functions. In pancreatic islets, CCK controls beta cell functions primarily through CCK1 receptors, but the signalling pathways downstream of these receptors in pancreatic beta cells are not well defined. EXPERIMENTAL APPROACH: Apoptosis in pancreatic beta cell apoptosis was evaluated using Hoechst-33342 staining, TUNEL assays and Annexin-V-FITC/PI staining. Insulin secretion and second messenger production were monitored using ELISAs. Protein and phospho-protein levels were determined by Western blotting. A glucose tolerance test was carried out to examine the functions of CCK-8s in streptozotocin-induced diabetic mice. KEY

resultsThe sulfated carboxy-terminal octapeptide CCK26-33 amide (CCK-8s) activated CCK1 receptors and induced accumulation of both IP3 and cAMP. Whereas Gq -PLC-IP3 signalling was required for the CCK-8s-induced insulin secretion under low-glucose conditions, Gs -PKA/Epac signalling contributed more strongly to the CCK-8s-mediated insulin secretion in high-glucose conditions. CCK-8s also promoted formation of the CCK1 receptor/β-arrestin-1 complex in pancreatic beta cells. Using β-arrestin-1 knockout mice, we demonstrated that β-arrestin-1 is a key mediator of both CCK-8s-mediated insulin secretion and of its the protective effect against apoptosis in pancreatic beta cells. The anti-apoptotic effects of β-arrestin-1 occurred through cytoplasmic late-phase ERK activation, which activates the 90-kDa ribosomal S6 kinase-phospho-Bcl-2-family protein pathway. CONCLUSIONS AND IMPLICATIONS: Knowledge of different CCK1 receptor-activated downstream signalling pathways in the regulation of distinct functions of pancreatic beta cells could be used to identify biased CCK1 receptor ligands for the development of new anti-diabetic drugs.

Indexed as

Signal TransductionAnimalsApoptosisArrestinsbeta-Arrestin 1beta-ArrestinsCholecystokininInsulinInsulin SecretionIslets of LangerhansMAP Kinase Signaling SystemMiceMice, KnockoutPhosphorylationReceptors, CholecystokininRibosomal Protein S6 Kinases, 90-kDaArrb1 protein, mouseArrestinsbeta-Arrestin 1beta-ArrestinsCholecystokininInsulinReceptors, CholecystokininRibosomal Protein S6 Kinases, 90-kDa

Identifiers

PMID26248680
PMCPMC4687794
OpenAlexW2167677329

What OpenQuestion holds

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Registered trials

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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.