Semaglutide peptide is a synthetic human glucagon-like peptide-1 (GLP-1) analog. GLP-1 peptide is an endogenous peptide hormone containing 30 amino acids. The primary function of this compound is to enhance insulin production, reduce blood sugar levels, and conserve the pancreatic beta cells by stimulating insulin gene transcription. Additionally, the compound delays gastric emptying and hence suppresses appetite. GLP-1 profoundly affects most critical organs, including the heart, kidney, lungs, and liver. Semaglutide, as a GLP-1 receptor agonist, can reduce insulin levels and glucose, reduce appetite, and help with weight loss.(1)
The peptide exerts its functions via various pathways, including:(2,3,4)
- Binding with the GLP-1 receptors, promoting glucose-dependent insulin release
- Suppressing the release of glucagon and inhibiting the hepatic synthesis of glucose
- Via pancreatic beta cell functioning, improving the proinsulin-to-insulin ratio in the subject
- Delaying gastric motility and reducing appetite for reduced body weight
Semaglutide Chemical Structure(5)
Molecular Formula: C187H291N45O59
Molecular Weight: 4114 g/mol
Other Titles: Glucagon-like peptide-1 (GLP-1)
Semaglutide Uses and Effects
Semaglutide and the Incretin Effect
An incretin is a group of hormones released by the gastrointestinal tract in response to meal intake, which helps decrease blood glucose levels. GLP-1 receptors are found on the surface of the beta cells in the pancreas. When the Semaglutide peptide binds, it stimulates insulin secretion and helps decrease the excess blood glucose levels.(1) As stated by J. J Holst, “The main actions of GLP-1 are to stimulate insulin secretion (i.e., to act as an incretin hormone) and to inhibit glucagon secretion, thereby contributing to limit postprandial glucose excursions.” Being a GLP-1 receptor agonist, Semaglutide peptide could contribute to the incretin hormone production and regulation of blood sugar levels.
Semaglutide and the Protection of Pancreatic Beta Cells
An experiment conducted on non-obese and diabetic mice models administered Semaglutide in combination with lisofylline (a compound that suppresses the autoimmune ability to combat diabetic conditions) and exedin-4 (a compound that assists the proliferation of beta cells).(6) The results demonstrated that the peptide promotes the growth of pancreatic beta cells and prevents cellular apoptosis. In addition to protecting the pancreatic beta cells, Semaglutide peptide helped maintain the optimal glucose levels in the body 145 days after the treatment was stopped.
Semaglutide and Appetite Suppression
GLP-1 receptor agonists such as Semaglutide delay gastric acid motility, contributing to satiation and reducing appetite.(1) Animal research models demonstrated that when administered in the brain, these peptides decrease the drive to consume food and prevent food intake.(7)
Semaglutide and Neurological Effects
The GLP-1 receptor, named GLP-1R, is vital in improving cognitive abilities. GLP-1 and GLP-1R are expressed in brain cells. When GLP-1R is deficient in the brain, it tends to cause seizures, impaired learning abilities, and neuronal injury. When bound to these receptors, it can improve cognitive and learning abilities. As per Mathew J During et al., “Systemic administration of GLP-1 receptor agonists in wild-type animals prevents kainate-induced apoptosis of hippocampal neurons. Brain GLP-1R represents a promising new target for cognitive-enhancing and neuroprotective agents.”(8) These results could indicate the potential of the peptide to treat cognitive ailments such as Alzheimer’s.
Semaglutide and Cardiovascular Effects
GLP-1 receptors are spread throughout the cardiovascular system, which, when activated, help maintain cardiac health.(9) GLP-1 and its agonists help maintain optimal blood pressure and reduce the left ventricular diastolic pressure, which, when not maintained, may lead to hypertrophy, cardiac issues, and heart attack. The Semaglutide peptide improves the glucose uptake of the heart muscles. Heart muscles become weak and ischemic post myocardial infarction, which can be reversed when administered with Semaglutide, thereby improving the cardiac condition.
- Mahapatra MK, Karuppasamy M, Sahoo BM. Semaglutide is a glucagon like peptide-1 receptor agonist with cardiovascular benefits for the management of type 2 diabetes. Rev Endocr Metab Disord. 2022 Jun;23(3):521-539. doi: 10.1007/s11154-021-09699-1. Epub 2022 Jan 7. PMID: 34993760; PMCID: PMC8736331. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8736331/
- Knudsen LB, Lau J. The Discovery and Development of Liraglutide and Semaglutide. Front Endocrinol (Lausanne). 2019 Apr 12;10:155. doi: 10.3389/fendo.2019.00155. PMID: 31031702; PMCID: PMC6474072. https://pubmed.ncbi.nlm.nih.gov/31031702/
- Ahmann AJ, Capehorn M, Charpentier G, Dotta F, Henkel E, Lingvay I, Holst AG, Annett MP, Aroda VR. Efficacy and Safety of Once-Weekly Semaglutide Versus Exenatide ER in Subjects With Type 2 Diabetes (SUSTAIN 3): A 56-Week, Open-Label, Randomized Clinical Trial. Diabetes Care. 2018 Feb;41(2):258-266. doi: 10.2337/dc17-0417. Epub 2017 Dec 15. PMID: 29246950. https://pubmed.ncbi.nlm.nih.gov/29246950/
- Christou GA, Katsiki N, Blundell J, Fruhbeck G, Kiortsis DN. Semaglutide as a promising antiobesity drug. Obes Rev. 2019 Jun;20(6):805-815. doi: 10.1111/obr.12839. Epub 2019 Feb 15. PMID: 30768766. https://pubmed.ncbi.nlm.nih.gov/30768766/
- National Center for Biotechnology Information (2022). PubChem Compound Summary for CID 56843331, Semaglutide. https://pubchem.ncbi.nlm.nih.gov/compound/Semaglutide
- Yang Z, Chen M, Carter JD, Nunemaker CS, Garmey JC, Kimble SD, Nadler JL. Combined treatment with lisofylline and exendin-4 reverses autoimmune diabetes. Biochem Biophys Res Commun. 2006 Jun 9;344(3):1017-22. doi: 10.1016/j.bbrc.2006.03.177. Epub 2006 Apr 5. PMID: 16643856. https://pubmed.ncbi.nlm.nih.gov/16643856/>
- Blonde L, Klein EJ, Han J, Zhang B, Mac SM, Poon TH, Taylor KL, Trautmann ME, Kim DD, Kendall DM. Interim analysis of the effects of exenatide treatment on A1C, weight and cardiovascular risk factors over 82 weeks in 314 overweight patients with type 2 diabetes. Diabetes Obes Metab. 2006 Jul;8(4):436-47. doi: 10.1111/j.1463-1326.2006.00602.x. PMID: 16776751. https://pubmed.ncbi.nlm.nih.gov/16776751/
- During MJ, Cao L, Zuzga DS, Francis JS, Fitzsimons HL, Jiao X, Bland RJ, Klugmann M, Banks WA, Drucker DJ, Haile CN. The glucagon-like peptide-1 receptor is involved in learning and neuroprotection. Nat Med. 2003 Sep;9(9):1173-9. doi: 10.1038/nm919. Epub 2003 Aug 17. PMID: 12925848. https://pubmed.ncbi.nlm.nih.gov/12925848/
- Gros R, You X, Baggio LL, Kabir MG, Sadi AM, Mungrue IN, Parker TG, Huang Q, Drucker DJ, Husain M. Cardiac function in mice lacking the glucagon-like peptide-1 receptor. Endocrinology. 2003 Jun;144(6):2242-52. doi: 10.1210/en.2003-0007. PMID: 12746281. https://pubmed.ncbi.nlm.nih.gov/12746281/
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Dr. Marinov (MD, Ph.D.) is a researcher and chief assistant professor in Preventative Medicine & Public Health. Prior to his professorship, Dr. Marinov practiced preventative, evidence-based medicine with an emphasis on Nutrition and Dietetics. He is widely published in international peer-reviewed scientific journals and specializes in peptide therapy research.