Glucagon-like peptide 1 (GLP-1) and Semaglutide are both small peptides. Studies suggest the major physiological purpose of the short, naturally occurring hormone is to reduce blood sugar levels by boosting insulin production. It has been linked to neurotrophic effects in the brain and central nervous system, and it seems to preserve beta-cell insulin reserves by boosting the transcription of insulin genes. Observations from research on the gastrointestinal system suggest that Semaglutide’s potential to decrease stomach emptying and stool movement may considerably reduce hunger. The proposed effects of Semaglutide on the heart, fat, muscles, bones, liver, lungs, and kidneys have all been hypothesized in preliminary investigations.
Semaglutide Peptide and Insulin Secretion
The “incretin effect,” as described by Holst, is the phenomenon most often linked to Semaglutide [i]. The digestive system secretes a class of metabolic hormones known as incretins, which operate together to reduce glucose (sugar) in the blood. Semaglutide seems one of two primary hormones (GIP) that may induce incretin activity as seem in murine models. Although GIP circulates at a concentration around ten times that of Semaglutide, some research suggests that GLP-1 may be more effective than GIP, particularly when blood glucose levels are high [ii].
Another interesting finding from this study is that “Decreased secretion of GLP-1 may contribute to the development of obesity, and exaggerated secretion may be responsible for postprandial reactive hypoglycemia.” Researchers hypothesize that Semaglutide may directly trigger insulin exocytosis from the pancreas by binding to receptors on the surface of pancreatic beta cells. Semaglutide, in addition to sulfonylurea, has been purported to boost insulin production. Protein synthesis, proteolysis, and amino acid absorption by skeletal muscle are all dietary consequences that might happen. It is speculated that the peptide may stimulate insulin synthesis in pancreatic beta cells and inhibit glucagon production in pancreatic alpha cells via interacting with GLP-1 receptors in the pancreas. The effects of Semaglutide seem to function in a glucose-dependent way, as suggested by the research teams investigating this possibility. In addition, findings imply the peptide may help mitigate the postprandial glucose surge that normally after food consumption. Following food intake, it may take longer for the stomach to empty (by as much as 38%, some studies suggest).
Semaglutide Peptide and Beta Cells
Animal studies on Semaglutide have suggested promise in promoting the development of new types of beta cells that are progenitors to the pancreatic duct epithelium. Researchers speculate that Semaglutide may also prevent beta-cell death. These impacts may disrupt the normal proportion of new beta cells to dying ones. These findings suggest that the peptide may one day mitigate diabetes and defend the pancreas against assaults that kill beta cells. Research suggests that Semaglutide may prevent beta-cell death brought on by an increase in inflammatory cytokines. Semaglutide seemed to protect islet cells from damage in type 1 diabetic mice models, suggesting it may be useful in practice for preventing the development of type 1 diabetes [iii]. The researchers said, “It is possible that such combined agents could become a new strategy to defeat T1DM.”
Semaglutide Peptide and Hunger
The infusion of Semaglutide into the brains of mice models has been suggested to lower the driving device and limit food intake [iv]. Semaglutide appears to cause satiety, which suppresses appetite. In recent research studies, the GLP-1 receptor agonist was suggested to promote progressive weight reduction in mice when presented for just two days. Due to this weight reduction, possible long-term properties include reduced cardiovascular risk factors and hemoglobin A1C levels.
GLP-1 receptor agonists have been suggested to have a role in appetite regulation, and research suggests that this may be due to their potential to activate GLP-1 receptors in the central nervous system, notably in reward-related brain regions [v]. More specifically, it is thought that neurons in the arcuate nucleus of the hypothalamus may interact with GLP-1 receptor agonists. These neurons are thought to express proopiomelanocortin and cocaine- and amphetamine-regulated transcript (POMC/CART), controlling appetite and hunger.
Semaglutide, a GLP-1 receptor agonist, has been hypothesized to stimulate satiety by potentially blocking the production of neuropeptide Y (NPY) and agouti-related peptide (AgRP), two peptides that are suggested to enhance appetite. Researchers speculate that GLP-1 receptor agonists like Semaglutide may help reduce the drop in free leptin and increase peptide YY (PYY) 3-36 levels to facilitate weight loss [vi]. One research suggested that when compared to a placebo, Semaglutide was associated with a 35% decrease in mean energy intake during ad libitum eating (1736kJ vs. 2676kJ).[vii]
Semaglutide Peptide and the Heart
Studies suggest Semaglutide-receptors may be found in the heart, and it seems that they may enhance cardiac function by boosting heart rate and decreasing left ventricular end-diastolic pressure under specific conditions. [viii] Left ventricular hypertrophy, cardiac remodeling, and heart failure are commonly linked to increased end-diastolic pressure. Semaglutide, as recent research suggests, may lessen the severity of heart attack damage. The peptide seems to enhance glucose absorption in the heart muscle, which may aid the ailing ischemic myocardium to perform normally and obtain the nutrients it needs to prevent programmed cell death.
Buy Semaglutide online if you are a licensed professional interested in further studying this compound.
[i] Holst JJ. From the Incretin Concept and the Discovery of GLP-1 to Today’s Diabetes Therapy. Front Endocrinol (Lausanne). 2019 Apr 26;10:260. doi: 10.3389/fendo.2019.00260. PMID: 31080438; PMCID: PMC6497767.
[ii] Holst JJ. The physiology of glucagon-like peptide 1. Physiol Rev. 2007 Oct;87(4):1409-39. doi: 10.1152/physrev.00034.2006. PMID: 17928588.
[iio] 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.
[iv] Tang-Christensen M, Larsen PJ, Thulesen J, Rømer J, Vrang N. The proglucagon-derived peptide, glucagon-like peptide-2, is a neurotransmitter involved in the regulation of food intake. Nat Med. 2000 Jul;6(7):802-7. doi: 10.1038/77535. PMID: 10888930.
[v] van Bloemendaal, L., IJzerman, R. G., Ten Kulve, J. S., Barkhof, F., Konrad, R. J., Drent, M. L., Veltman, D. J., & Diamant, M. (2014). GLP-1 receptor activation modulates appetite- and reward-related brain areas in humans. Diabetes, 63(12), 4186–4196. https://doi.org/10.2337/db14-0849
[vi] Ard, J., Fitch, A., Fruh, S., & Herman, L. (2021). Weight Loss and Maintenance Related to the Mechanism of Action of Glucagon-Like Peptide 1 Receptor Agonists. Advances in therapy, 38(6), 2821–2839. https://doi.org/10.1007/s12325-021-01710-0
[vii] Friedrichsen, M., Breitschaft, A., Tadayon, S., Wizert, A., & Skovgaard, D. (2021). The effect of semaglutide 2.4 mg once weekly on energy intake, appetite, control of eating, and gastric emptying in adults with obesity. Diabetes, obesity & metabolism, 23(3), 754–762. https://doi.org/10.1111/dom.14280
[viii] 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.