Semaglutide and Liraglutide are two peptides that have made a major impression on the research community due to their potential to induce substantial weight reduction and possible research applicability within the context of metabolic syndrome. Despite all the buzz around peptides, they are not the only novel compounds scientists are exploring. GLP-1 analogs like Semaglutide have received much attention. However, this may change as more is learned about other molecules like Tesofensine and the need for innovative research in metabolic syndrome grows.
What is Semaglutide Peptide?
Studies indicate that Semaglutide, as a GLP-1 agonist, may function similarly to glucagon-like peptide-1 (GLP-1), a hormone secreted by the intestines that controls blood sugar levels and hunger. Semaglutide is an incretin mimic since GLP-1 is an incretin. Semaglutide, Liraglutide, Dulaglutide, Albiglutide, Tirzepatide, and Exenatide are all examples of incretin mimetics that have been hypothesized to be effective in the context of type 2 diabetes through potentially enhancing glycemic control, facilitating weight reduction, and decreasing cardiovascular risk factors.
Researchers speculate that GLP-1 agonists may enhance insulin secretion by binding to GLP-1 receptors on pancreatic beta cells. By encouraging muscle cell glucose absorption and suppressing hepatic glucose synthesis, this rise in insulin may contribute to glycemic control.
Investigations purport that GLP-1 may influence insulin secretion and act on the brain and spinal cord. As they may bind to GLP-1 receptors in the brain, particularly the hypothalamus, GLP-1 agonists may induce hormone signaling affecting food intake.
What is Tesofensine Peptide?
Tesofensine, an investigational SNDRI (serotonin-norepinephrine-dopamine reuptake inhibitor), may induce a reduction in food intake and raising basal metabolic rate, studies suggest. Tesofensine’s mechanism of action is believed to be similar to that of antidepressants; however, most antidepressants control the absorption of serotonin and norepinephrine, or sometimes only serotonin. Nonetheless, Tesofensine’s potential in dopamine reuptake piqued researchers’ attention as a possible research compound in studies of Parkinson’s disease.
Research suggests that Tesofensine’s potential in regulating hormone signals controlling food intake may originate from its alleged capacity to block the reuptake of norepinephrine and dopamine. Tesofensine may influence the reward and satiety circuits in the brain, resulting in decreased food intake.
Semaglutide vs. Tesofensine
The potential impact of Semaglutide on weight reduction has been extensively studied in experimental studies. As findings suggested, Semaglutide appeared to have led to a weight reduction of almost 8% compared to a weight increase of nearly 7% in the placebo group in a 20-week trial. These results suggest that Semaglutide may aid weight loss when other parameters, are constant. Semaglutide has been speculated to cause significantly more weight reduction than placebo (6%) during two to three months study durations.
Early clinical studies using Tesofensine focused on its potential in the context of Alzheimer’s and Parkinson’s illnesses, and it was suggested that the substance may have caused considerable weight loss as a side effect. Because of this finding, Tesofensine has been studied as a possible weight-reduction agent.
Tesofensine and Semaglutide have been purported to exhibit comparable effects in terms of their size. Unfortunately, comparing these two molecules is difficult because test settings have varied greatly for both. One promising avenue for future study would be directly comparing the two in well-designed comparative animal experiments. A more direct analysis might be produced at that point, and comparing the kind and extent of off-target effects may be feasible.
Tesofensine and Semaglutide: Mechanism of Action
Tesofensine and Semaglutide are not the same thing at all. Studies suggest that Tesofensine may modulate neurotransmitter levels, while Semaglutide is a GLP-1 mimic that may bind to the GLP-1 receptor in different organs. In contrast to Tesofensine, which isn’t a peptide, Semaglutide is a synthetic peptide. Tesofensine is a tiny molecule chemical that may be considered an octane.
Research suggests that there are at least three methods through which Semaglutide, a synthetic counterpart of GLP-1, may affect weight. First, the gastrointestinal (GI) incretin hormone GLP-1 is critical in controlling blood sugar levels. GLP-1 and GIP (glucose-dependent insulinotropic peptide) have been purported to stimulate the pancreas’ insulin production. The trophic properties of elevated insulin secretion may include increased protein synthesis, decreased protein breakdown, and improved amino acid absorption by skeletal muscle. Insulin (and, by extension, GLP-1) is speculated to help suppress the release of certain hormones that signal hunger and prevent the breakdown of fat.
However, GLP-1 receptors are not exclusive to the pancreas. Studies have suggested activating GLP-1 receptors in the brain might decrease appetite. More studies on mice purported that GLP-1 may increase fullness and decrease cravings, which are considered responsible for food-seeking behavior. Research has also suggested that Semaglutide may decrease binge-like behaviors by modifying neurotransmission in the brain’s reward areas or suppressing neuronal activity in the amygdala.
Thirdly, GLP-1 has been hypothesized to encourage weight reduction by decreasing the rate at which food moves through the digestive system. As a side effect of slowing the GI system to improve nutrition absorption, there is a release of stretch receptors, which convey messages to the brain mitigating food seeking patterns.
Intriguingly, Semaglutide may be in the business of balancing energy levels by limiting consumption. Tesofensine may have a similar purpose, albeit through dissimilar methods.
Tesofensine’s mechanism of action is less studied than Semaglutide. Tesofensine seems to act on various brain and central nervous system receptors. First, it probably inhibits hunger by binding to alpha-1 adrenoceptors. Researchers speculate that it most likely exerts a comparable, though milder, impact through binding to the dopamine D1 receptor. The research proposes that Tesofensine “tricks” the brain into believing the GI tract is full by mimicking the dopamine signaling present after satiety.
Scientists interested in further research can buy Semaglutide peptide from Biotech Peptides’ website, for the highest quality research compounds.
[i] Novo Nordisk A/S, “Effect and Safety of Semaglutide 2.4 mg Once-weekly in Subjects With Overweight or Obesity,” clinicaltrials.gov, Clinical trial registration NCT03548935, Nov. 2021. Accessed: Jun. 13, 2023. [Online].
[ii] D. Rubino et al., “Effect of Continued Weekly Subcutaneous Semaglutide vs Placebo on Weight Loss Maintenance in Adults With Overweight or Obesity: The STEP 4 Randomized Clinical Trial,” JAMA, vol. 325, no. 14, pp. 1414–1425, Apr. 2021, doi: 10.1001/jama.2021.3224.
[iii] A. Astrup, S. Madsbad, L. Breum, T. J. Jensen, J. P. Kroustrup, and T. M. Larsen, “Effect of tesofensine on bodyweight loss, body composition, and quality of life in obese patients: a randomised, double-blind, placebo-controlled trial,” Lancet Lond. Engl., vol. 372, no. 9653, Art. no. 9653, 29 2008, doi: 10.1016/S0140-6736(08)61525-1.
[iv] V. Chuong et al., “The glucagon-like peptide-1 (GLP-1) analogue semaglutide reduces alcohol drinking and modulates central GABA neurotransmission,” JCI Insight, May 2023, doi: 10.1172/jci.insight.170671.
[v] C. Aranäs et al., “Semaglutide reduces alcohol intake and relapse-like drinking in male and female rats,” EBioMedicine, vol. 93, p. 104642, Jun. 2023, doi: 10.1016/j.ebiom.2023.104642.