In one paragraphArticle in Diabetologia, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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 registryThe 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 literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
14 authors.
Ying Liu *Department of Endocrinology and Metabolism of Huashan Hospital, State Key Laboratory of Brain Function and Disorders, MOE Frontiers Center for Brain Science and the Institutes of Brain Science, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0002-9341-2674 Yunzhi Ni *Department of Endocrinology and Metabolism of Huashan Hospital, State Key Laboratory of Brain Function and Disorders, MOE Frontiers Center for Brain Science and the Institutes of Brain Science, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0003-2453-2522 Chuantong Xie *Department of Endocrinology and Metabolism of Huashan Hospital, State Key Laboratory of Brain Function and Disorders, MOE Frontiers Center for Brain Science and the Institutes of Brain Science, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0002-9012-1345 Linling Fan *Department of Endocrinology and Metabolism of Huashan Hospital, State Key Laboratory of Brain Function and Disorders, MOE Frontiers Center for Brain Science and the Institutes of Brain Science, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0002-1239-2713 Quanya SunDepartment of Endocrinology and Metabolism of Huashan Hospital, State Key Laboratory of Brain Function and Disorders, MOE Frontiers Center for Brain Science and the Institutes of Brain Science, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0002-8446-4480 Bei MaoDepartment of Endocrinology and Metabolism of Huashan Hospital, State Key Laboratory of Brain Function and Disorders, MOE Frontiers Center for Brain Science and the Institutes of Brain Science, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0002-8537-8701 Chuxin HuangDepartment of Endocrinology and Metabolism of Huashan Hospital, State Key Laboratory of Brain Function and Disorders, MOE Frontiers Center for Brain Science and the Institutes of Brain Science, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0003-3649-0497 Zhaoyun ZhangDepartment of Endocrinology and Metabolism of Huashan Hospital, State Key Laboratory of Brain Function and Disorders, MOE Frontiers Center for Brain Science and the Institutes of Brain Science, Fudan University, Shanghai, China.
Yehong YangDepartment of Endocrinology and Metabolism of Huashan Hospital, State Key Laboratory of Brain Function and Disorders, MOE Frontiers Center for Brain Science and the Institutes of Brain Science, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0003-3600-2174 Min HeDepartment of Endocrinology and Metabolism of Huashan Hospital, State Key Laboratory of Brain Function and Disorders, MOE Frontiers Center for Brain Science and the Institutes of Brain Science, Fudan University, Shanghai, China. hemin2@huashan.org.cn.ORCID http://orcid.org/0009-0007-1879-838X Lei XiaoDepartment of Endocrinology and Metabolism of Huashan Hospital, State Key Laboratory of Brain Function and Disorders, MOE Frontiers Center for Brain Science and the Institutes of Brain Science, Fudan University, Shanghai, China. leixiao@fudan.edu.cn.ORCID http://orcid.org/0000-0002-6897-4608 Yiming LiDepartment of Endocrinology and Metabolism of Huashan Hospital, State Key Laboratory of Brain Function and Disorders, MOE Frontiers Center for Brain Science and the Institutes of Brain Science, Fudan University, Shanghai, China. yimingli@fudan.edu.cn.ORCID http://orcid.org/0000-0002-1828-8765 Rui LiuDepartment of Endocrinology and Metabolism of Huashan Hospital, State Key Laboratory of Brain Function and Disorders, MOE Frontiers Center for Brain Science and the Institutes of Brain Science, Fudan University, Shanghai, China. fd_ruiliu@fudan.edu.cn.ORCID http://orcid.org/0000-0002-8321-1617 Funding
Ministry of Science and Technology of the People's Republic of China 82200949Ministry of Science and Technology of the People's Republic of China 82300954Noncommunicable Chronic Diseases-National Science and Technology Major Project 2023ZD0506800
6 · The paper itselfAbstract
aims/hypothesisG-protein-coupled receptors (GPCRs) play an important role in maintaining systemic glucose homeostasis by regulating insulin secretion, with protein kinase A (PKA) signalling serving as a key downstream effector. Our previous work identified specific expression of type IIB PKA in pancreatic beta cells. Based on these findings, we propose that type IIB PKA is involved in mediating the GPCR signalling in pancreatic beta cells.
methodsThe glucagon-like peptide-1 (GLP-1) analogue liraglutide was administered to mice 30 min before glucose injection during an IPGTT, whereas the glucose levels and insulin levels were measured in wild-type and RIIβ-knockout mice. The isolated islets were subjected to both perifusion assay and static batch incubations following stimulation with liraglutide, glucagon and follicle-stimulating hormone (FSH). RNA-seq analysis was performed to identify molecular changes in islets with RIIβ ablation. Both western blotting and quantitative PCR were employed to quantify the gene expression. Whole-cell patch-clamp recordings were conducted to measure K
resultsRIIβ-knockout mice exhibited impaired glucose tolerance and attenuated insulin secretion in response to liraglutide. Islets isolated from RIIβ-knockout mice showed reduced insulin secretion following liraglutide stimulation. Similarly, RIIβ-ablated islets displayed decreased insulin secretion in response to both glucagon and FSH. Further mechanistic studies revealed that RIIβ deficiency impaired liraglutide-mediated PKA signalling activation. Specifically, RIIβ-ablated beta cells exhibited reduced basal K CONCLUSIONS/
interpretationOur results highlight type IIB PKA as a primary mediator of Gs-coupled receptor-potentiated insulin secretion, providing a new molecular framework for metabolic regulation research.
Indexed as
Cyclic AMP-Dependent Protein KinasesInsulinReceptors, G-Protein-CoupledAnimalsGlucagon-Like Peptide 1Insulin-Secreting CellsInsulin SecretionLiraglutideMaleMiceMice, Inbred C57BLMice, KnockoutSignal TransductionCyclic AMP-Dependent Protein KinasesGlucagon-Like Peptide 1InsulinLiraglutideReceptors, G-Protein-CoupledGlucagon-like peptide-1G-protein-coupled receptorInsulin secretionProtein kinase A
Identifiers
PMID42337176
PMCPMC13424381
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