Semaglutide (GLP-1) (3mg & 5mg)

What is the Semaglutide (GLP-1) peptide?

Semaglutide (GLP-1) and glucagon-like peptide 1 are short, natural peptides. The naturally occurring hormone is only 3031 amino acids in length, with a primary physiological function to lower blood sugar levels by naturally increasing insulin secretion. It also appears to protect beta-cell insulin stores by promoting transcription of insulin genes, and is associated with neurotrophic effects in the central nervous system and the brain. Studies in the GI system have observed that Semaglutide may significantly reduce appetite by slowing gastric emptying and bowel motility. Preliminary studies have also suggested potential 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 Research

Semaglutide and the Incretin Effect
According to Holst, the most widespread association with Semaglutide is the “incretin effect.”^[1] Incretins are a group of metabolic hormones released from the gastrointestinal tract that lower blood sugar (sugar) levels. Semaglutide appears to be 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 may be more potent than GIP, especially when blood glucose levels are relatively high.^[2] The researcher also notes that “Decreased secretion of GLP-1 may contribute to the development of obesity, and exaggerated secretion may be responsible for postprandial reactive hypoglycemia.” Semaglutide receptors have been identified on the surface of pancreatic beta cells, suggesting that Semaglutide may directly stimulate insulin exocytosis from the pancreas. In combination with the sulfonylurea substance, Semaglutide has been suggested to increase insulin secretion. Various potential nutritional effects include a possible increase in protein synthesis, decreased proteolysis, and increase in amino acid uptake by skeletal muscle.

Semaglutide and Beta Cell Protection
Studies in animal models suggest that Semaglutide may stimulate the growth and proliferation of pancreatic beta cells and the differentiation of new forms of beta cells, precursors of pancreatic duct epithelium. Studies further theorize that Semaglutide may inhibit beta-cell apoptosis. These effects have the potential to upset the average balance between beta-cell growth and death. In terms of development, these research results posit the peptide’s potential to treat diabetes and protect the pancreas from attacks that damage beta cells. One particularly compelling study has indicated that Semaglutide appears to inhibit beta-cell death caused by elevated levels of inflammatory cytokines. In fact, in type 1 mouse models with diabetes, it was observed that Semaglutide appeared to protects islet cells from destruction, and therefore it may be a valuable tool in practice to prevent the onset of type 1 diabetes.^[3] The scientists suggested that “It is possible that such combined therapy could become a new strategy to defeat T1DM in humans.”

Semaglutide and Appetite
A study of mouse models suggests that administration of Semaglutide in the brain of mice may reduce the driving device and may inhibit food intake.^[4] Semaglutide seems to induce satiation, reducing hunger instincts. Recent clinical trials are shown in the mouse where two-day management of the GLP-1 receptor agonist may cause gradual weight loss. This weight loss may lead to 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 appear to improve cardiac function in certain situations by increasing heart rate and lowering left ventricular end-diastolic pressure.^[5] A rise in end-diastolic pressure is often associated with left ventricular hypertrophy, cardiac remodeling, and ultimate heart failure. Recent studies suggest that Semaglutide may reduce the overall damage caused by a heart attack. The peptide appears 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 exhibited apparent improved and reduced LV performance and systemic vascular resistance. The latter effect may help lower blood pressure and relieve stress. This process, in turn, may help 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 appeared to improve myocardial performance in both experimental animal models and patients.

Semaglutide and the Brain
There is potential evidence that Semaglutide may help to enhance learning and protect neurons from neurodegenerative diseases such as Alzheimer’s. One study has posited that Semaglutide may enhance associative and spatial learning in mice and improve learning disabilities in mice with specific gene defects. In rats that overexpress Semaglutide receptors in particular brain areas, both learning and memory appear to be significantly better than normal controls.^[6] Further research studies of mice indicated the peptide’s potential to protect from immunotoxic neurons. Interestingly, Semaglutide and its analog exendin-4 have been reported in mouse models to apparently 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.^[7]
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. Semaglutide (GLP-1) has so far been reported to exhibit minimal to moderate side effects and low oral and excellent subcutaneous bioavailability in mice, according to laboratory studies.^[8]

References