Phospholipase C‐β1 potentiates glucose‐stimulated insulin secretion
Abstract
PLC-β exerts biologic influences through GPCR. GPCRs are involved in regulating glucose-stimulated insulin secretion (GSIS). Previous studies have suggested that PLC-βs might play an important role in pancreatic β cells. However, because of a lack of the specific inhibitors of PLC-β isozymes and appropriate genetic models, the in vivo function of specific PLC-β isozymes in pancreatic β cells and their physiologic relevance in the regulation of insulin secretion have not been studied so far. The present study showed that PLC-β1 was crucial for β-cell function by generation of each PLC-β conditional knockout mouse. Mice lacking PLC-β1 in β cells exhibited a marked defect in GSIS, leading to glucose intolerance. In ex vivo studies, the secreted insulin level and Ca 2+ response in Plcb1 f/f ; pancreas/duodenum homeobox protein 1 ( Pdx1 )-Cre recombinase-estrogen receptor T2 ( CreERt2 ) islets was lower than those in the Plcb1 f/f islets under the high-glucose condition. PLC-β1 led to potentiate insulin secretion via stimulation of particular G q -protein-coupled receptors. Plcb1 f/f ; Pdx1-CreERt2 mice fed a high-fat diet developed more severe glucose intolerance because of a defect in insulin secretion. The present study identified PLC-β1 as an important molecule that regulates β cell insulin secretion and can be considered a candidate for therapeutic intervention in diabetes mellitus.-Hwang, H.-J., Yang, Y. R., Kim, H. Y., Choi, Y., Park, K.-S., Lee, H., Ma, J. S., Yamamoto, M.…
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PLCβ1 has been implicated in control of neuronal function and enhancement of glucose-stimulated insulin secretion in pancreatic β-cells downstream of specific GPCRs.
“Among many roles, ubiquitously expressed PLCβ1 enzyme has been implicated in control of neuronal function and the enhancement of glucose-stimulated insulin secretion in pancreatic β-cells downstream of specific GPCRs in these different cell types [36–40].”
From Phosphatidylinositol(4,5)bisphosphate: diverse functions at the plasma membrane (2020) · cites this paper as [39]
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- Authors
- Hwang, H.-J., Yang, Y. R., Kim, H. Y., Choi, Y., Park, K.-S., Lee, H., Ma, J. S., Yamamoto, M., Kim, J., Chae, Y. C., Choi, J. H., Cocco, L., Berggren, P.-O., Jang, H.-J., & Suh, P.-G.
- Affiliations
- Ulsan National Institute of Science and Technology (KR)
- Korea Research Institute of Bioscience and Biotechnology (KR)
- School of Life Sciences Ulsan National Institute of Science and Technology Ulsan South Korea
- National Cancer Center (KR)
- Department of Immunoparasitology Research Institute for Microbial Diseases Osaka University Suita Japan
- Research Institute for Microbial Diseases, The University of Osaka (JP)
- Pohang University of Science and Technology (KR)
- University of Bologna (IT)
- Corresponding author
- Jang, Hyun-Jun
- Suh, Pann-Ghill
- ORCID
- Venue
- The FASEB Journal
- Publisher
- Wiley
- Published
- 2019-07-03
- Volume
- 33
- Issue
- 10
- Pages
- 10668-10679
- ISSN
- 0892-6638 (ISSN-L)
- 1530-6860
- OpenAlex
- W2955901650
- Cited by
- 20
- References
- 55
- Citations by year
- 2026: 3 · 2025: 1 · 2023: 1 · 2022: 5 · 2021: 5 · 2020: 5
- FWCI
- 3.82
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The FASEB Journal (publishedVersion)
- PubMed (publishedVersion)
- Archivio istituzionale della ricerca (Alma Mater Studiorum Università di Bologna) (submittedVersion)
- KRIBB Repository (submittedVersion)
- Scholarworks@UNIST (Ulsan National Institute of Science and Technology) (submittedVersion)
- Funders
- National Science Foundation, United Arab Emirates (NRF-2014M3A9D8034456, NRF-2017R1E1A1A01074510)
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- PLCB1, glucose-stimulated insulin secretion, pancreatic beta cells, G protein-coupled receptors, Gq protein, conditional knockout mice, impaired glucose tolerance, high-fat diet, diabetes mellitus, insulin secretion, calcium response
- MeSH terms
- Insulin Secretion, Animals, Cell Line, Glucose, Islets of Langerhans, Isoenzymes, Male, Mice, Inbred C57BL, Trans-Activators, Glucose Intolerance, Mice, Knockout, Homeodomain Proteins, Receptors, G-Protein-Coupled, Insulin-Secreting Cells, Mice, Phospholipase C beta, Diet, High-Fat, In Vitro Techniques
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