Semaglutide

Semaglutide is a GLP-1 analog that lowers glucose, suppresses appetite, promotes weight loss, and improves cardiovascular and hepatic health. It also shows neuroprotective potential in Parkinson’s and Alzheimer’s.

- Improve metabolic and cardiovascular health

- Manage obesity or insulin resistance

Mechanism of Action

How this peptide works in the body

Glycemic Control:

Semaglutide binds to GLP-1 receptors (GLP-1R) on pancreatic β-cells, activating the cAMP/PKA pathway, which enhances glucose-dependent insulin secretion. This prevents excessive insulin release, reducing the risk of hypoglycemia. Simultaneously, it suppresses glucagon secretion from pancreatic α-cells by inhibiting cAMP production, limiting hepatic gluconeogenesis and glycogenolysis, thereby lowering fasting and postprandial blood glucose levels.

Appetite Suppression:

Semaglutide activates GLP-1 receptors in the arcuate nucleus (ARC) of the hypothalamus, stimulating pro-opiomelanocortin (POMC) neurons while inhibiting agouti-related peptide (AgRP) neurons, reducing hunger signals. This modulation decreases neuropeptide Y (NPY) release, suppressing appetite. Additionally, it delays gastric emptying by reducing vagal signaling and inhibiting gastric antral motility, prolonging satiety and reducing caloric intake.

Cardiometabolic Effects:

Semaglutide improves lipid metabolism by downregulating hepatic sterol regulatory element-binding proteins (SREBPs), reducing triglyceride and LDL cholesterol synthesis while promoting fatty acid oxidation. It attenuates systemic inflammation by inhibiting nuclear factor kappa B (NF-κB) signaling, reducing the production of proinflammatory cytokines (IL-6, TNF-α, CRP). This contributes to decreased vascular inflammation, endothelial dysfunction, and atherosclerotic plaque formation, lowering cardiovascular risk.

Weight Loss:

Semaglutide's dual effects on appetite and metabolism lead to sustained fat loss. It enhances lipolysis and β-oxidation in adipose tissue by modulating AMPK and PPAR-α activity, increasing energy expenditure. Additionally, its impact on dopaminergic reward circuits in the ventral tegmental area (VTA) reduces food cravings and compulsive eating behaviors, supporting long-term weight management.