Semaglutide (GLP-1) (3mg)

What Is Semaglutide (GLP-1) Peptide?

Semaglutide (GLP-1) and glucagon-like peptide 1 are short, naturally occurring peptides. The hormone is only 3031 amino acids in length. Its primary physiological function is to lower blood sugar levels by naturally increasing insulin secretion. It also protects beta-cell insulin stores by promoting transcription of insulin genes and is associated with neurotrophic effects in the central nervous system and the brain. The GI system has shown that Semaglutide significantly reduces appetite by slowing gastric emptying and bowel motility. Preliminary studies have also demonstrated the effects of Semaglutide on the heart, fat, muscles, bones, liver, lungs, lungs, and kidneys.

Specifications

Synonyms: GLP-1, proglucagon (72-108), glucagon-like peptide-1

Molecular Formula: C187H291N45O59

Molecular Weight: 4113.64 g/mol

Sequence: HXEGTFTSDV SSYLEGQAAK EFIAWLVRGR G

PubChem: CID 56843331

CAS Number: 910463-68-2

Reconstitution: Required

Semaglutide (GLP-1) Research

The Incretin Effect of Semaglutide
According to Holst, it’s probably the most critical effect of Semaglutide, which was named the “incretin effect.” Incretins are a group of metabolic hormones released from the gastrointestinal tract that lower blood sugar (sugar) levels. Semaglutide is one of the two most common and essential hormones that stimulate incretin action in the rodent model (the other is GIP).
GIP circulates at about 10 times the concentration of Semaglutide, but there is evidence that GLP-1 is more potent than GIP, especially when blood glucose levels are relatively high.
Semaglutide receptors have been identified on the surface of pancreatic beta cells, indicating that Semaglutide directly stimulates insulin exocytosis from the pancreas. In combination with the sulfonylurea substance, Semaglutide has been shown to increase insulin secretion sufficient to induce mild insulin secretion. Hypoglycemia is in up to 40% of subjects. Increased insulin secretion is associated with this. Various nutritional effects include increased protein synthesis, decreased proteolysis, and increased amino acid uptake by skeletal muscle.

Semaglutide and Beta Cell Protection
Studies in animal models suggest that Semaglutide can stimulate the growth and proliferation of pancreatic beta cells and the differentiation of new forms of beta cells, precursors of pancreatic duct epithelium. Studies also show that Semaglutide inhibits beta-cell apoptosis. These effects upset the average balance between beta-cell growth and death. For development, it suggests that peptides may help treat diabetes and protect the pancreas from attacks that damage beta cells.
One particularly compelling study has shown that Semaglutide inhibits beta-cell death caused by elevated levels of inflammatory cytokines. In fact, in type 1 mouse models with diabetes, it is demonstrated that Semaglutide protects islet cells from destruction and may be a valuable tool in practice to prevent the onset of type 1 diabetes.

Semaglutide and Appetite
The study of mouse models suggests that administration of Semaglutide in the brain of mice can reduce the driving device and can inhibit food supply. Semaglutide seems to improve saturation to help people feel indirect and reduce hunger. Recent clinical trials are shown in the mouse where two-day management of the GLP-1 receptor agonist causes gradual weight loss. This weight loss is associated with a significant improvement in cardiovascular risk factors and a decrease in hemoglobin A1C mirror for a long time.

Potential Cardiovascular Benefits of Semaglutide
Currently, Semaglutide receptors are distributed throughout the heart and improve cardiac function in certain situations by increasing heart rate and lowering left ventricular end-diastolic pressure. The latter does not seem to be so, but the rise in end-diastolic pressure is associated with left ventricular hypertrophy, cardiac remodeling, and ultimate heart failure. Recent evidence suggests that Semaglutide may reduce the overall damage caused by a heart attack. Peptides appear to improve glucose uptake into the heart muscle; this helps the struggling ischemic myocardium maintain function and obtain the nutrients needed to avoid programmed cell death. Increased glucose uptake in these cells appears to be independent of insulin.
High doses of Semaglutide in dogs have improved and reduced LV performance and systemic vascular resistance. The latter effect helps lower blood pressure and relieve stress. This process, in turn, helps reduce the long-term consequences such as LV remodeling, vascular thickening, and heart failure. According to Dr. Horst, administration of GLP-1 after heart injury consistently improved myocardial performance in both experimental animal models and patients.

Semaglutide and the Brain
There is evidence that Semaglutide helps enhance learning and protect neurons from neurodegenerative diseases such as Alzheimer’s. One study has shown that Semaglutide enhances associative and spatial learning in mice and improves learning disabilities in mice with specific gene defects. In rats that overexpress Semaglutide receptors in particular brain areas, both learning and memory are significantly better than normal controls.
Further research studies of mice showed that it could help protect from immunotoxic neurons. Neurodegeneration damage to glutamine formation, full protective board model. The apoptotic sys peptide may even stimulate neurite protrusions in cultured cells.
Interestingly, Semaglutide and its analog exendin-4 have been shown in mouse models to reduce amyloid-beta levels in the brain. The beta-amyloid precursor protein found in neurons is the primary component of the plaques observed in Alzheimer’s disease.
It remains to be seen if preventing amyloid-beta accumulation can protect against the effects of Alzheimer’s disease. Still, this research is, at the very least, a tantalizing clue as to how scientists may intervene in the progression of mild cognitive impairment to whole Alzheimer’s disease.
GLP-1 exhibits minimal to moderate side effects and low oral and excellent subcutaneous bioavailability in mice.