Semaglutide is a by-product of GLP-1, a naturally occurring peptide speculated to reduce the amount of sugar in the blood and increase the amount of insulin shed. Research indicates that Semaglutide, an analog of GLP-1, may have the potential to enhance the function of the heart, liver, and lungs, in addition to assisting in the slowing or prevention of the symptoms of Alzheimer's disease. It has been hypothesized that GLP-1 may considerably reduce hunger by delaying the emptying of the stomach and lowering the motility of the intestinal tract. Modifications have been made to GLP-1 in the hopes of establishing a longer half-life and more favorable pharmacokinetics.
GLP-1 Peptide Introduction
GLP-1, an abbreviation for glucagon-like peptide-1, is a naturally occurring peptide hormone that is just 30–31 amino acids in length. Its major physiological purpose is theorized to be to reduce the amount of sugar in the blood by naturally increasing the amount of insulin secreted. Additionally, it has been connected with neurotrophic effects in the brain and central nervous system, and it may play a function in preserving beta cell insulin reserves by stimulating the transcription of the insulin gene. In the gastrointestinal tract, it has been speculated that GLP-1 may dramatically reduce hunger by delaying stomach emptying and lowering intestinal tract motility. It has been ascertained via a preliminary study that GLP-1 might have an effect not just on the heart but also on fat, muscles, bones, liver, lungs, and kidneys.
The management and prevention of diabetes and the reduction of hunger have been the key areas of concentration for research into GLP-1. Secondary study focuses on the practical effects that the peptide may have on the cardiovascular system. The potential of GLP-1 in neurodegenerative disease is the subject of research that is more recent and, as a result, less comprehensive. Even though this last field of research is the most recent, it is also the domain of GLP-1 study that is expanding at a rapid pace. This is because it has been asserted that the peptide may either slow down or prevent the production of amyloid beta plaques in the context of Alzheimer's disease.
GLP-1 Peptide and the Brain
Some data suggests that GLP-1 may increase learning and help protect neurons against neurodegenerative disorders like Alzheimer's. This is supported by the fact that GLP-1 has been speculated to have these effects. According to one research study, GLP-1 seems to correct learning deficiencies in mice with certain gene abnormalities and boost associative and spatial learning in mice. Learning and memory appear to be greatly improved in rats with overexpression of the GLP-1 receptor in certain brain parts. This is in comparison to rat control models.
Further studies on mice have implied that GLP-1 may protect against excitotoxic neuron damage. Furthermore, it has been indicated that GLP-1 might protect rat models of neurodegeneration from glutamate-induced apoptosis. The peptide has been hypothesized to induce neurite outgrowth in cells that have been grown. According to the researchers, further investigation on GLP-1 is expected to provide light on the potential use of this protein in the context or reversal of certain neurodegenerative illnesses.
Interestingly, GLP-1 for sale and its counterpart, exendin-4, has been purported to lower levels of amyloid-beta in the brain of mice models, in addition to the beta-amyloid precursor protein present in neurons. Amyloid beta is the principal component of the plaques detected in Alzheimer's disease. These plaques, although related to the severity of the illness, are not necessarily recognized as the cause of the disease. It is not yet known whether or not inhibiting the formation of amyloid beta will protect against the consequences of Alzheimer's disease; nonetheless, this discovery provides, at the very least, a fascinating indication as to how scientists may intervene in the development of moderate cognitive impairment to full Alzheimer's disease.
GLP-1 Peptide Potential
It has been theorized that GLP-1 receptors are dispersed throughout the heart and may enhance cardiac performance under certain circumstances. This is hypothesized to be accomplished by increasing the heart rate and decreasing the end-diastolic pressure of the left ventricle. The latter may not seem very significant, yet an increase in the end-diastolic pressure of the left ventricle (LV) is linked to LV hypertrophy, cardiac remodeling, and, ultimately, heart failure.
Recent research has even indicated that GLP-1 could play a role in reducing the total damage that is produced by a heart attack. It would seem that the peptide may enhance the absorption of glucose by cardiac muscle, which in turn assists ischemic heart muscle cells that are operating poorly in getting the nourishment they need to continue functioning and escape programmed cell death. It would indicate that insulin is not responsible for the increase in glucose absorption in these cells.
There is data suggesting that giving large concentrations of GLP-1 to dogs may increase the left ventricle (LV) performance and lower systemic vascular resistance. Due to this latter impact, blood pressure may be lowered, reducing the strain on the heart. As a result, this may assist in preventing the long-term repercussions of high blood pressure, which include remodeling of the left ventricle (LV), thickening of the arterial walls, and heart failure. Since the presentation of GLP-1 after cardiac damage has "constantly increased myocardial performance in experimental animal models," Dr. Holst has said this has been the case.
References
[i] "The Physiology of Glucagon-like Peptide 1 | Physiological Reviews." [Online].
[ii] "Combined treatment with lisofylline and exendin-4 reverses autoimmune diabetes. — PubMed — NCBI." [Online].
[iii] "The proglucagon-derived peptide, glucagon-like peptide-2, is a neurotransmitter involved in the regulation of food intake. — PubMed — NCBI." [Online].
[iv] "Interim analysis of the effects of exenatide treatment on A1C, weight and cardiovascular risk factors over 82 weeks in 314 overweight patients with... — PubMed — NCBI." [Online].
[v] "Cardiac function in mice lacking the glucagon-like peptide-1 receptor. — PubMed — NCBI." [Online].
