ArticleBritish journal of pharmacology2012
β(2)-Adrenoceptors increase translocation of GLUT4 via GPCR kinase sites in the receptor C-terminal tail.
Article in British journal of pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 36 citations in OpenAlex.
- WNKs regulate mouse behavior and alter central nervous system glucose uptake and insulin signaling.bioRxiv : the preprint server for biology · 2025Article
- The dual GLP-1 and GIP receptor agonist tirzapetide provides an unintended interaction with the β-adrenoceptors and plays a role in glucose metabolism in hyperglycemic or senescent cardiac cells.Cardiovascular diabetology · 2025Article
- Melanocortin-4 Receptor PLC Activation Is Modulated by an Interaction with the Monocarboxylate Transporter 8.International journal of molecular sciences · 2024Article
- Role of G protein-coupled receptor kinases (GRKs) in βPharmacology research & perspectives · 2024Article
- Muscle-specific deletion ofFrontiers in endocrinology · 2022Article
- The β2-adrenergic receptor in the apical membrane of intestinal enterocytes senses sugars to stimulate glucose uptake from the gut.Frontiers in cell and developmental biology · 2022Article
- Re-Evaluating the Oxidative Phenotype: Can Endurance Exercise Save the Western World?Antioxidants (Basel, Switzerland) · 2021Review
- GluT4: A central player in hippocampal memory and brain insulin resistance.Experimental neurology · 2020Review
- Adrenoceptor regulation of the mechanistic target of rapamycin in muscle and adipose tissue.British journal of pharmacology · 2019Review
- Preassembled GPCR signaling complexes mediate distinct cellular responses to ultralow ligand concentrations.Science signaling · 2018Article
- Evidence of G-protein-coupled receptor and substrate transporter heteromerization at a single molecule level.Cellular and molecular life sciences : CMLS · 2018Article
- The Role of G Protein-coupled Receptor Kinases in Cancer.International journal of biological sciences · 2018Review
- Novel Roles for the Insulin-Regulated Glucose Transporter-4 in Hippocampally Dependent Memory.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- The neuroenergetics of stress hormones in the hippocampus and implications for memory.Frontiers in neuroscience · 2015Review
- The endogenous molecular clock orchestrates the temporal separation of substrate metabolism in skeletal muscle.Skeletal muscle · 2015Article
- β2-adrenoceptor agonists can both stimulate and inhibit glucose uptake in mouse soleus muscle through ligand-directed signalling.Naunyn-Schmiedeberg's archives of pharmacology · 2013Article
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeβ-Adrenoceptor stimulation induces glucose uptake in several insulin-sensitive tissues by poorly understood mechanisms. EXPERIMENTAL APPROACH: We used a model system in CHO-K1 cells expressing the human β(2)-adrenoceptor and glucose transporter 4 (GLUT4) to investigate the signalling mechanisms involved. KEY
resultsIn CHO-K1 cells, there was no response to β-adrenoceptor agonists. The introduction of β(2)-adrenoceptors and GLUT4 into these cells caused increased glucose uptake in response to β-adrenoceptor agonists. GLUT4 translocation occurred in response to insulin and β(2)-adrenoceptor stimulation, although the key insulin signalling intermediate PKB was not phosphorylated in response to β(2)-adrenoceptor stimulation. Truncation of the C-terminus of the β(2)-adrenoceptor at position 349 to remove known phosphorylation sites for GPCR kinases (GRKs) or at position 344 to remove an additional PKA site together with the GRK phosphorylation sites did not significantly affect cAMP accumulation but decreased β(2)-adrenoceptor-stimulated glucose uptake. Furthermore, inhibition of GRK by transfection of the βARKct construct inhibited β(2)-adrenoceptor-mediated glucose uptake and GLUT4 translocation, and overexpression of a kinase-dead GRK2 mutant (GRK2 K220R) also inhibited GLUT4 translocation. Introducing β(2)-adrenoceptors lacking phosphorylation sites for GRK or PKA demonstrated that the GRK sites, but not the PKA sites, were necessary for GLUT4 translocation. CONCLUSIONS AND IMPLICATIONS: Glucose uptake in response to activation of β(2)-adrenoceptors involves translocation of GLUT4 in this model system. The mechanism is dependent on the C-terminus of the β(2)-adrenoceptor, requires GRK phosphorylation sites, and involves a signalling pathway distinct from that stimulated by insulin.
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