No products in the cart
Semaglutide’s Potential for Weight Management and Appetite Control
Semaglutide is a peptide and a prescription medication available in both US and EU for managing type 2 diabetes and obesity.
The medication is an agonist to the glucagon-like peptide-1 (GLP-1) receptors in the pancreas, the brain, and other organs. The effects of the drug are similar to GLP-1, a peptide hormone naturally produced by the intestines. It’s an incretin, meaning it stimulates insulin secretion.
Depending on the dosage, Semaglutide peptide can have different benefits, which range from reducing blood sugar levels and improving pancreatic beta cell function to suppressing appetite and supporting weight loss.
Semaglutide is also a subject of extensive research regarding other potential benefits, such as reducing pancreatic beta cell apoptosis and exhibiting neuroprotective properties.
Blood Sugar Control
Research involving Semaglutide to manage high blood sugar in patients with type 2 diabetes is currently ongoing. It works by activating the GLP-1 receptors in the pancreatic beta cells, stimulating insulin synthesis and release.
The stimulating effect on insulin synthesis is the primary mechanism via which Semaglutide lowers both fasting and postprandial glucose levels.
A meta-analysis of 26 RCTs reveals that oral and injectable Semaglutide can effectively lower the fasting blood sugar levels and markers for long-term glucose control, such as HbA1c, in patients with type 2 diabetes.
In addition to stimulating insulin secretion, Semaglutide reduces glucagon release and suppresses hepatic gluconeogenesis. These effects are confirmed by studies in non-diabetic patients, which lasted up to 12 weeks and showed over 38% reduction in blood sugar levels compared to a placebo after a carbohydrate-rich breakfast.
The researchers also report that Semaglutide effectively slowed the speed of gastric emptying during the first hour after a meal compared to a placebo.
The scientists suggested that this effect of Semaglutide may contribute to a more gradual release of glucose into the blood after a meal and better glycemic control. Yet, the overall speed of gastric emptying over the entire 5-hour monitoring period after the meal was not affected.
A significant factor that helps Semaglutide stand out is that it can reduce hyperglycemia without causing hypoglycemia.
The risk of hypoglycemia is not higher when compared to a placebo because Semaglutide stimulates insulin secretion in a glucose-dependent manner. In addition, the inhibition of glucagon release also does not occur under hypoglycemic conditions.
Semaglutide’s potential for weight management and appetite control
Another significant advantage of Semaglutide over other medications for diabetes is that it can stimulate insulin secretion without leading to weight gain. Research shows that individuals with diabetes experience weight loss while taking the medication.
Studies show that Semaglutide significantly reduces ad libitum energy intake, which can result in weight loss in the long term. In one trial, obese individuals lost 5 kg on average for 12 weeks without restricting their energy intake.
According to the study, Semaglutide reduced hunger and food cravings, improved control of eating, and reduced the patient’s preference for high-fat foods. This resulted in a 24% reduction in daily energy intake.
Semaglutide can help reduce hunger and cravings by activating the GLP-1 receptors in the brain, which play a major role in modulating appetite and reward-related behavior.
Furthermore, the potential of Semaglutide to slow down gastric emptying within the first hour of having a meal may also contribute to a reduced ad libitum energy intake.
Stimulation of pancreatic beta cell survival and proliferation
Preliminary studies conducted in vitro and in test animals reveal that Semaglutide may stimulate pancreatic beta cells’ survival and proliferation.
These potential effects are of significant interest since patients with type 2 diabetes often suffer pancreatic beta cell dysfunction and apoptosis in the long term.
Animal research suggests that Semaglutide may help reverse the harmful changes of obesity and insulin resistance on pancreatic beta cells and stimulate their proliferation. It is important to note that human beta cells have a limited capacity to increase.
Researchers reveal that many in vitro studies also report that GLP-1 antagonists, such as Semaglutide, may protect pancreatic beta cells from apoptosis.
Several potential mechanisms are involved in the protective effect of Semaglutide, and one of the most prominent is reducing the overload on the endoplasmic reticulum of the beta cells in diabetic conditions.
GLP-1 receptor activation may also help stimulate autophagy, which prevents beta cell injury and death by protecting against inflammation and oxidative stress.
Although many of these studies are in human islets, human studies are lacking, and the relevance of these mechanisms for type 2 diabetes patients remains to be proven. This is because technologies to assess in 3D the correct beta cell mass in vivo in humans are yet to be developed.
Semaglutide and the potential neuroprotective benefits
Interestingly, Parkinson’s disease and type 2 diabetes share several genetic susceptibilities, such as single nucleotide polymorphisms in the growth factor signaling kinase gene Akt. This has sparked interest in researching the potential effects of diabetes medications for managing Parkinson’s disease.
Currently, other GLP-1 receptor agonists, such as Exendin-4, have already shown protective effects on Parkinson’s patients in phase II clinical trials. The benefits lasted up to 3 months after discontinuing the medication.
Another GLP-1 antagonist, Liraglutide, is currently being tested in a phase II trial in Parkinson’s patients.
The research regarding the potential neuroprotective effects of Semaglutide is still in its infancy, but many laboratory studies in animal models of PD show promising results. The experiments report that Semaglutide has neuroprotective effects and increases the survival of the dopaminergic neurons, the apoptosis of which is associated with the development of Parkinson’s.
In animals, Semaglutide alleviated the chronic inflammatory responses in the brain, reduced lipid peroxidation, and increased the expression of growth factors that protect dopaminergic neurons in the substantia nigra and striatum.
Disclaimer: The products mentioned are not intended for human or animal consumption. Research chemicals are intended solely for laboratory experimentation and/or in-vitro testing. Bodily introduction of any sort is strictly prohibited by law. All purchases are limited to licensed researchers and/or qualified professionals. All information shared in this article is for educational purposes only.
- Dhillon S. Semaglutide: First Global Approval. Drugs. 2018 Feb;78(2):275-284. DOI: 10.1007/s40265-018-0871-0. PMID: 29363040.
- Hou Y, Ernst SA, Heidenreich K, Williams JA. Glucagon-like peptide-1 receptor is present in pancreatic acinar cells and regulates amylase secretion through cAMP. Am J Physiol Gastrointest Liver Physiol. 2016 Jan 1;310(1):G26-33. doi: 10.1152/ajpgi.00293.2015. Epub 2015 Nov 5. PMID: 26542397; PMCID: PMC4698438.
- Zaazouee MS, Hamdallah A, Helmy SK, Hasabo EA, Sayed AK, Gbreel MI, Elmegeed AA, Aladwan H, Elshanbary AA, Abdel-Aziz W, Elshahawy IM, Rabie S, Elkady S, Ali AS, Ragab KM, Nourelden AZ. Semaglutide for the treatment of type 2 Diabetes Mellitus: A systematic review and network meta-analysis of safety and efficacy outcomes. Diabetes Metab Syndr. 2022 Jun;16(6):102511. DOI: 10.1016/j.dsx.2022.102511. Epub 2022 May 20. PMID: 35623229.
- Mahapatra MK, Karuppasamy M, Sahoo BM. Semaglutide, a glucagon like peptide-1 receptor agonist with cardiovascular benefits for 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.
- Hjerpsted JB, Flint A, Brooks A, Axelsen MB, Kvist T, Blundell J. Semaglutide improves postprandial glucose and lipid metabolism, and delays first-hour gastric emptying in subjects with obesity. Diabetes Obes Metab. 2018 Mar;20(3):610-619. DOI: 10.1111/dom.13120. Epub 2017 Oct 27. PMID: 28941314; PMCID: PMC5836914.
- Smits MM, Van Raalte DH. Safety of Semaglutide. Front Endocrinol (Lausanne). 2021 Jul 7;12:645563. doi: 10.3389/fendo.2021.645563. Erratum in: Front Endocrinol (Lausanne). 2021 Nov 10;12:786732. PMID: 34305810; PMCID: PMC8294388.
- Mares AC, Chatterjee S, Mukherjee D. Semaglutide for weight loss and cardiometabolic risk reduction in overweight/obesity. Curr Opin Cardiol. 2022 Jul 1;37(4):350-355. DOI: 10.1097/HCO.0000000000000955. Epub 2022 Feb 16. PMID: 35175229.
- Blundell J, Finlayson G, Axelsen M, Flint A, Gibbons C, Kvist T, Hjerpsted JB. Effects of once-weekly Semaglutide on appetite, energy intake, control of eating, food preference and body weight in subjects with obesity. Diabetes Obes Metab. 2017 Sep;19(9):1242-1251. DOI: 10.1111/dom.12932. Epub 2017 May 5. PMID: 28266779; PMCID: PMC5573908.
- van Bloemendaal L, IJzerman RG, Ten Kulve JS, Barkhof F, Konrad RJ, Drent ML, Veltman DJ, Diamant M. GLP-1 receptor activation modulates appetite- and reward-related brain areas in humans. Diabetes. 2014 Dec;63(12):4186-96. DOI: 10.2337/db14-0849. Epub 2014 Jul 28. PMID: 25071023.
- Tomita T. Apoptosis in pancreatic β-islet cells in Type 2 diabetes. Bosn J Basic Med Sci. 2016 Aug 2;16(3):162-79. DOI: 10.17305/bjbms.2016.919. Epub 2016 May 22. PMID: 27209071; PMCID: PMC4978108.
- Marinho TS, Martins FF, Cardoso LEM, Aguila MB, Mandarim-de-Lacerda CA. Pancreatic islet cells disarray, apoptosis, and proliferation in obese mice. The role of Semaglutide treatment. Biochimie. 2022 Feb;193:126-136. doi: 10.1016/j.biochi.2021.10.017. Epub 2021 Nov 4. PMID: 34742857.
- Costes S, Bertrand G, Ravier MA. Mechanisms of Beta-Cell Apoptosis in Type 2 Diabetes-Prone Situations and Potential Protection by GLP-1-Based Therapies. Int J Mol Sci. 2021 May 18;22(10):5303. doi: 10.3390/ijms22105303. PMID: 34069914; PMCID: PMC8157542.
- Xiromerisiou G, Hadjigeorgiou GM, Papadimitriou A, Katsarogiannis E, Gourbali V, Singleton AB. Association between AKT1 gene and Parkinson’s disease: a protective haplotype. Neurosci Lett. 2008 May 9;436(2):232-4. doi: 10.1016/j.neulet.2008.03.026. Epub 2008 Mar 15. PMID: 18395980; PMCID: PMC8958471.
- Athauda D, Maclagan K, Skene SS, Bajwa-Joseph M, Letchford D, Chowdhury K, Hibbert S, Budnik N, Zampedri L, Dickson J, Li Y, Aviles-Olmos I, Warner TT, Limousin P, Lees AJ, Greig NH, Tebbs S, Foltynie T. Exenatide once weekly versus placebo in Parkinson’s disease: a randomised, double-blind, placebo-controlled trial. Lancet. 2017 Oct 7;390(10103):1664-1675. DOI: 10.1016/S0140-6736(17)31585-4. Epub 2017 Aug 3. PMID: 28781108; PMCID: PMC5831666.
- Zhang L, Zhang L, Li L, Hölscher C. Semaglutide is Neuroprotective and Reduces α-Synuclein Levels in the Chronic MPTP Mouse Model of Parkinson’s Disease. J Parkinsons Dis. 2019;9(1):157-171. DOI: 10.3233/JPD-181503. PMID: 30741689.
- Clinical trial identifier NCT02953665
Dr. Usman (BSc, MBBS, MaRCP) completed his studies in medicine at the Royal College of Physicians, London. He is an avid researcher with more than 30 publications in internationally recognized peer-reviewed journals. Dr. Usman has worked as a researcher and a medical consultant for reputable pharmaceutical companies such as Johnson & Johnson and Sanofi.