The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.
A Role for β-Cell-Expressed G Protein-Coupled Receptor 119 in Glycemic Control by Enhancing Glucose-Dependent Insulin Release
Abstract
Pancreatic β-cell dysfunction is a hallmark event in the pathogenesis of type 2 diabetes. Injectable peptide agonists of the glucagon-like peptide 1 (GLP-1) receptor have shown significant promise as antidiabetic agents by virtue of their ability to amplify glucose-dependent insulin release and preserve pancreatic β-cell mass. These effects are mediated via stimulation of cAMP through β-cell GLP-1 receptors. We report that the Gαs-coupled receptor GPR119 is largely restricted to insulin-producing β-cells of pancreatic islets. Additionally, we show here that GPR119 functions as a glucose-dependent insulinotropic receptor. Unlike receptors for GLP-1 and other peptides that mediate enhanced glucose-dependent insulin release, GPR119 was suitable for the development of potent, orally active, small-molecule agonists. The GPR119-specific agonist AR231453 significantly increased cAMP accumulation and insulin release in both HIT-T15 cells and rodent islets. In both cases, loss of GPR119 rendered AR231453 inactive. AR231453 also enhanced glucose-dependent insulin release in vivo and improved oral glucose tolerance in wild-type mice but not in GPR119-deficient mice. Diabetic KK/Ay mice were also highly responsive to AR231453. Orally active GPR119 agonists may offer significant promise as novel antihyperglycemic agents acting in a glucose-dependent fashion.
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Cohen, L. J., Esterhazy, D., Kim, S.-H., Lemetre, C., Aguilar, R. R., Gordon, E. A., Pickard, A. J., Cross, J. R., Emiliano, A. B., Han, S. M., et al. (2017) · Nature · doi:10.1038/nature23874 · Cited by 500
Artmann, A., Petersen, G., Hellgren, L. I., Boberg, J., Skonberg, C., Nellemann, C., Hansen, S. H., & Hansen, H. S. (2008) · Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids · doi:10.1016/j.bbalip.2008.01.006 · Cited by 287
Sonoda, N., Imamura, T., Yoshizaki, T., Babendure, J. L., Lu, J.-C., & Olefsky, J. M. (2008) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0710402105 · Cited by 239
Metadata
- Authors
- Chu, Z.-L., Jones, R. M., He, H., Carroll, C., Gutierrez, V., Lucman, A., Moloney, M., Gao, H., Mondala, H., Bagnol, D., Unett, D., Liang, Y., Demarest, K., Semple, G., Behan, D. P., & Leonard, J.
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2007-06-01
- Volume
- 148
- Issue
- 6
- Pages
- 2601-2609
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- OpenAlex
- W2096726403
- Cited by
- 294
- References
- 3
- FWCI
- 18.96
- Type
- journal article
- Language
- en
- Open access
- closed
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- Chu, Z.-L., Jones, R. M., He, H., Carroll, C., Gutierrez, V., Lucman, A., Moloney, M., Gao, H., Mondala, H., Bagnol, D., Unett, D., Liang, Y., Demarest, K., Semple, G., Behan, D. P., & Leonard, J. (2007). A Role for β-Cell-Expressed G Protein-Coupled Receptor 119 in Glycemic Control by Enhancing Glucose-Dependent Insulin Release. Endocrinology. https://doi.org/10.1210/en.2006-1608
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
