ArticleDiabetologia2014
β-Arrestin2 plays a key role in the modulation of the pancreatic beta cell mass in mice.
Article in Diabetologia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 56 citations in OpenAlex.
- GPCR Biased Signaling in Metabolism.Handbook of experimental pharmacology · 2026Review
- Multi-faceted roles of β-arrestins in G protein-coupled receptor endocytosis.Nature communications · 2025Article
- GLP1R and GIPR expression and signaling in pancreatic alpha cells, beta cells and delta cells.Peptides · 2024Article
- Divergent acute versus prolonged pharmacological GLP-1R responses in adult β cell-specific β-arrestin 2 knockout mice.Science advances · 2023Article
- Islet MC4R Regulates PC1/3 to Improve Insulin Secretion in T2DM Mice via the cAMP and β-arrestin-1 Pathways.Applied biochemistry and biotechnology · 2022Article
- The therapeutic potential of GLP-1 receptor biased agonism.British journal of pharmacology · 2022 · on this mapReview
- Tertiary butylhydroquinone alleviated liver steatosis and increased cell survival via β-arrestin-2/PI3K/AKT pathway.Iranian journal of basic medical sciences · 2021Article
- β-arrestin 2 is essential for fluoxetine-mediated promotion of hippocampal neurogenesis in a mouse model of depression.Acta pharmacologica Sinica · 2021Article
- Revisiting the Complexity of GLP-1 Action from Sites of Synthesis to Receptor Activation.Endocrine reviews · 2021Review
- GRK2 regulates GLP-1R-mediated early phase insulin secretion in vivo.BMC biology · 2021Article
- Beneficial metabolic role of β-arrestin-1 expressed by AgRP neurons.Science advances · 2020Article
- Metabolic effects of skeletal muscle-specific deletion of beta-arrestin-1 and -2 in mice.PLoS genetics · 2019Article
- Single-cell transcriptomics unveils gene regulatory network plasticity.Genome biology · 2019Article
- Article
- Scaffold Proteins: From Coordinating Signaling Pathways to Metabolic Regulation.Endocrinology · 2018Review
- β-arrestin-2 is an essential regulator of pancreatic β-cell function under physiological and pathophysiological conditions.Nature communications · 2017Article
- Deletion of β-Arrestin2 in Mice Limited Pancreatic β-Cell Expansion under Metabolic Stress through Activation of the JNK Pathway.Molecular medicine (Cambridge, Mass.) · 2016Article
- Inhibition of the MAP3 kinase Tpl2 protects rodent and human β-cells from apoptosis and dysfunction induced by cytokines and enhances anti-inflammatory actions of exendin-4.Cell death & disease · 2016Article
- β-Arrestin Recruitment and Biased Agonism at Free Fatty Acid Receptor 1.The Journal of biological chemistry · 2015Article
- Review
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisBeta cell failure due to progressive secretory dysfunction and limited expansion of beta cell mass is a key feature of type 2 diabetes. Beta cell function and mass are controlled by glucose and hormones/neurotransmitters that activate G protein-coupled receptors or receptor tyrosine kinases. We have investigated the role of β-arrestin (ARRB)2, a scaffold protein known to modulate such receptor signalling, in the modulation of beta cell function and mass, with a specific interest in glucagon-like peptide-1 (GLP-1), muscarinic and insulin receptors.
methodsβ-arrestin2-knockout mice and their wild-type littermates were fed a normal or a high-fat diet (HFD). Glucose tolerance, insulin sensitivity and insulin secretion were assessed in vivo. Beta cell mass was evaluated in pancreatic sections. Free cytosolic [Ca(2+)] and insulin secretion were determined using perifused islets. The insulin signalling pathway was evaluated by western blotting.
resultsArrb2-knockout mice exhibited impaired glucose tolerance and insulin secretion in vivo, but normal insulin sensitivity compared with wild type. Surprisingly, the absence of ARRB2 did not affect glucose-stimulated insulin secretion or GLP-1- and acetylcholine-mediated amplifications from perifused islets, but it decreased the islet insulin content and beta cell mass. Additionally, there was no compensatory beta cell mass expansion through proliferation in response to the HFD. Furthermore, Arrb2 deletion altered the islet insulin signalling pathway. CONCLUSIONS/
interpretationARRB2 is unlikely to be involved in the regulation of insulin secretion, but it is required for beta cell mass plasticity. Additionally, we provide new insights into the mechanisms involved in insulin signalling in beta cells.
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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.