GLP-1
From Proteopedia
(Difference between revisions)
| Line 22: | Line 22: | ||
== Consequences of receptor binding == | == Consequences of receptor binding == | ||
| - | In the pancreas, GLP-1 plays a critical role in glucose regulation through its glucose-dependent insulin secretion. It stimulates insulin release only when blood glucose levels are elevated, preventing hypoglycemia. In the brain, GLP-1 receptor agonists play a significant role in regulating feeding behaviors and appetite | + | In the pancreas, GLP-1 plays a critical role in glucose regulation through its glucose-dependent insulin secretion. It stimulates insulin release only when blood glucose levels are elevated, preventing hypoglycemia. In the brain, GLP-1 receptor agonists play a significant role in regulating feeding behaviors and appetite<ref>PMID: 34975402</ref>. In the heart, GLP-1 receptor activation has several cardio-protective effects. It reduces oxidative stress (unstable molecules with not enough antioxidants to neutralize) and improves cardiac function during low blood flow events. These and other actions make GLP-1 beneficial for patients with type 2 diabetes or cardiovascular disease<ref>PMID: 17928588</ref>. |
| - | + | ||
== Student contributors == | == Student contributors == | ||
| - | + | This page was created as a two-week project of an undergraduate biochemistry course. Karsten Theis would like to acknowledge contributors Jamie, Trey, Spencer, Pam, Summer, and Hyancinth Osei. | |
</StructureSection> | </StructureSection> | ||
== References == | == References == | ||
<references/> | <references/> | ||
Revision as of 21:01, 20 December 2024
Glucagon-like peptide 1 (GLP-1) is a hormone involved in insulin regulation. It was discovered when researchers found that glucose in the digestive tract led to higher insulin levels than the same amount of glucose administered directly in the blood stream[1]. GLP-1 is produced in specialized cells in the intestine and in the pancreas, is released into the blood and has effects on cells in the pancreas, in the brain, and in many other organs. The half-life of GLP-1 is on the order of minutes, so it exerts a short-term effect unless continuously produced.
| |||||||||||
References
- ↑ Müller TD, Finan B, Bloom SR, D'Alessio D, Drucker DJ, Flatt PR, Fritsche A, Gribble F, Grill HJ, Habener JF, Holst JJ, Langhans W, Meier JJ, Nauck MA, Perez-Tilve D, Pocai A, Reimann F, Sandoval DA, Schwartz TW, Seeley RJ, Stemmer K, Tang-Christensen M, Woods SC, DiMarchi RD, Tschöp MH. Glucagon-like peptide 1 (GLP-1). Mol Metab. 2019 Dec;30:72-130. PMID:31767182 doi:10.1016/j.molmet.2019.09.010
- ↑ doi: https://dx.doi.org/10.1002/mrc.880
- ↑ Ali S, Drucker DJ. Benefits and limitations of reducing glucagon action for the treatment of type 2 diabetes. Am J Physiol Endocrinol Metab. 2009 Mar;296(3):E415-21. PMID:19116373 doi:10.1152/ajpendo.90887.2008
- ↑ Ramzy A, Kieffer TJ. Altered islet prohormone processing: a cause or consequence of diabetes? Physiol Rev. 2022 Jan 1;102(1):155-208. PMID:34280055 doi:10.1152/physrev.00008.2021
- ↑ Chen XY, Chen L, Yang W, Xie AM. GLP-1 Suppresses Feeding Behaviors and Modulates Neuronal Electrophysiological Properties in Multiple Brain Regions. Front Mol Neurosci. 2021 Dec 17;14:793004. PMID:34975402 doi:10.3389/fnmol.2021.793004
- ↑ Holst JJ. The physiology of glucagon-like peptide 1. Physiol Rev. 2007 Oct;87(4):1409-39. PMID:17928588 doi:10.1152/physrev.00034.2006
