Semaglutide (GLP-1) – 3MG/5MG/10MG
$101.00 – $207.00
Discount per Quantity
| Quantity | Discount | Price |
|---|---|---|
| 5 - 8 | 5% | $95.95 – $196.65 |
| 9 + | 10% | $90.90 – $186.30 |
Semaglutide is a GLP-1 receptor agonist (GLP-1RA) that is based on the structure of naturally occurring human glucagon-like peptide 1 (GLP-1). AbstractGLP-1 is a 30-31 amino acid peptide hormone. Latest studies indicate that the major effect of this molecule is an increase in insulin secretion, a decrease in glycemia, and a preservation of pancreatic beta cells as well as stimulation of transcription of the insulin gene, [5] In addition, this compound seems to a delay in gastric emptying mediated by appetite suppression and decrease in calories intake. The authors of this Original Investigation hypothesized that semaglutide, a GLP-1 receptor agonist, could slow gastric emptying and the appearance of glucose, resulting in increased meal-induced satiety and weight loss. The peptide can act through several pathways e.g;
Peptide is taken to develop potential with different pathways like:
- May be also agonizing GLP-1 receptors found in the pancreatic tissues, disseminating glucose-dependent insulin episode.
- Theoretical-may suppress glucagon release and limit hepatic synthesis of glucose.
- This may occur through working on the pancreatic beta cell, improving the proinsulin-to-insulin ratio
- Perhaps by slowing gastric motility, stimulating satiety producing centres and suppressing appetite influences
In this patient, Semaglutide caused impaired gastric acid motility which might have lead to early satiation and hence suppressed appetite. Research has suggested that it slows gastric emptying in the postprandial period, possibly by up to a 38% slowing in the first ~2 hours post-dose which leads to earlier satiety and reduced desire for food. Additionally, prior research has shown that these peptides may reduce the motivation to eat when administered in the brain and decrease food intake. Specifically, the data suggest a possible connection between GLP-1 receptor activation in reward circuits of the brain and the appetite attenuation seen with Semaglutide. The hypothesis states that GLP-1 receptor agonists, like Semaglutide, might interact with specific neurons in the arcuate nucleus of the hypothalamus. GLP-1 receptor agonists interact with hypothalamic peptides through a complex neurochemical pathway. These neurons are located within the arcuate nucleus, a key hub of the neuroendocrine system that is an integrator of peripheral energy-state signals and promotes behavioral and physiological responses to adapt to or withstand energetic challenges. Those neurons are thought to be heavily involved in controlling appetite and hunger. It has been postulated that they are POMC/CART expressing. This activation of those POMC/CART neurons by Semaglutide could potentially enhance satiety and indirectly suppress the release of neuropeptide Y (NPY) and agouti-related peptide (AgRP), two hunger-related peptides. There is also speculation that on periods of weight loss, such agents (GLP-1 receptor agonists like semaglutide) could potentiate the decrease in free leptin levels and actually increase PepTYPYYtoonekghree-listo-sizay. The collective evidence suggests that Semaglutide remains a potent appetite suppressant. In a related study, more than a third of Semaglutide may allow an average reduction in meal energy intake with freely available food by 35%, compared to a placebo (1736kJ vs. 2676kJ).
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