The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Glucagon-like Peptide 1 Can Directly Protect the Heart Against Ischemia/Reperfusion Injury
Open accessAbstract
Glucagon-like peptide 1 (GLP-1), a gut incretin hormone that stimulates insulin secretion, also activates antiapoptotic signaling pathways such as phosphoinositide 3-kinase and mitogen-activated protein kinase in pancreatic and insulinoma cells. Since these kinases have been shown to protect against myocardial injury, we hypothesized that GLP-1 could directly protect the heart against such injury via these prosurvival signaling pathways. Both isolated perfused rat heart and whole animal models of ischemia/reperfusion were used, with infarct size measured as the end point of injury. In both studies, GLP-1 added before ischemia demonstrated a significant reduction in infarction compared with the valine pyrrolidide (an inhibitor of its breakdown) or saline groups. This protection was abolished in the in vitro hearts by the GLP-1 receptor antagonist exendin (9-39), the cAMP inhibitor Rp-cAMP, the PI3kinase inhibitor LY294002, and the p42/44 mitogen-activated protein kinase inhibitor UO126. Western blot analysis demonstrated the phosphorylation of the proapoptotic peptide BAD in the GLP-1–treated groups. We show for the first time that GLP-1 protects against myocardial infarction in the isolated and intact rat heart. This protection appears to involve activating multiple prosurvival kinases. This finding may represent a new therapeutic potential for this class of drug currently undergoing clinical trials in the treatment of type 2 diabetes.
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Cites
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Glucagon-like Peptide-1 Receptor Signaling Modulates β Cell Apoptosis
Li, Y., Hansotia, T., Yusta, B., Ris, F., Halban, P. A., & Drucker, D. J. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m209423200 · Cited by 589
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Hansotia, T., Baggio, L. L., Delmeire, D., Hinke, S. A., Yamada, Y., Tsukiyama, K., Seino, Y., Holst, J. J., Schuit, F., & Drucker, D. J. (2004) · Diabetes · doi:10.2337/diabetes.53.5.1326 · Cited by 309
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“The GLP-1 receptor is a G protein–coupled receptor and is a distinct member of the glucagon-secretin receptor super family that has been shown to function by causing intracellular calcium influx in addition to upregulating cAMP (3).”
BackgroundBarragán, J. M., Eng, J., Rodríguez, R., & Blázquez, E. (1999) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1999.277.5.e784 · Cited by 142
Cited by
Yellon, D. M., & Hausenloy, D. J. (2007) · New England Journal of Medicine · doi:10.1056/nejmra071667 · Cited by 3,797
Self-citationBiology of Incretins: GLP-1 and GIP
Baggio, L. L., & Drucker, D. J. (2007) · Gastroenterology · doi:10.1053/j.gastro.2007.03.054 · Cited by 3,639
The Physiology of Glucagon-like Peptide 1
Holst, J. J. (2007) · Physiological Reviews · doi:10.1152/physrev.00034.2006 · Cited by 3,371
The biology of incretin hormones
Drucker, D. J. (2006) · Cell Metabolism · doi:10.1016/j.cmet.2006.01.004 · Cited by 2,210
Glucagon-like peptide 1 (GLP-1)
Müller, T. D., Finan, B., Bloom, S. R., D'Alessio, D., Drucker, D. J., Flatt, P. R., Fritsche, A., Gribble, F., Grill, H. J., Habener, J. F., et al. (2019) · Molecular Metabolism · doi:10.1016/j.molmet.2019.09.010 · Cited by 1,868
Metadata
- Authors
- Bose, A. K., Mocanu, M. M., Carr, R. D., Brand, C. L., & Yellon, D. M.
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2005-01-01
- Volume
- 54
- Issue
- 1
- Pages
- 146-151
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2134141467
- Cited by
- 638
- References
- 9
- FWCI
- 15.41
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Bose, A. K., Mocanu, M. M., Carr, R. D., Brand, C. L., & Yellon, D. M. (2005). Glucagon-like Peptide 1 Can Directly Protect the Heart Against Ischemia/Reperfusion Injury. Diabetes. https://doi.org/10.2337/diabetes.54.1.146
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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