/ 20 February 2024

Studying peptides and weight: Semaglutide research

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There is also a possibility that GLP-1 may improve cognitive and cardiac performance

One of the most prominent incretin hormones, GLP-1, has been hypothesised to promote increased insulin secretion (glucose-dependent), decrease hepatic gluconeogenesis, and inhibit glucagon release. In addition, it has been speculated to reduce hunger and energy intake and delay stomach emptying. Research suggests that HbA1c levels and weight was reduced via peptide activity in obese research models of type 2 diabetes.

A significant hurdle to its efficacy is its short half-life of 1-2 minutes, caused by Dipeptidyl Peptidase-4 (DPP-4) and Neutral Endopeptidase-mediated destruction. Consequently, several GLP-1 receptor agonists were developed to mimic GLP-1’s action while being resistant to proteolytic degradation. These include Dulaglutide, Liraglutide, and Semaglutide. Options based on Exendin (Exenatide, Lixisenatide) and GLP-1 analogs (Liraglutide, Semaglutide, and Dulaglutide) are examples of GLP-1 receptor agonists that have been theorised to find relevance in research within this specific sector.

Semaglutide peptide research

Semaglutide and obesity

Scientists examined the potential of Semaglutide in the context of obesity research. From the beginning until the completion of the study period, the researchers tracked how much weight the animal research models lost or gained. Researchers then compared the weight reduction rates of two groups: one getting the novel peptide Semaglutide and another receiving a “dummy” adjuvant. Research models were also put under strict dietary conditions and increased physical activity, in addition to being given the peptide. The random assignment of research models to either Semaglutide or a placebo determined the course of the experiment.

Semaglutide peptide and cognitive action

Some research suggests that GLP-1 may help mitigate neurodegenerative illnesses like Alzheimer’s and enhance learning. One research purported that Semaglutide may improve learning deficiencies in mice with certain genetic abnormalities and improve associative and spatial learning in regular mice. Learning and memory seem much improved in rats compared to their normal counterparts when the Semaglutide receptor is overexpressed in certain brain areas.

In addition to shielding rat models of neurodegeneration from glutamate-induced apoptosis, further mouse research has indicated that Semaglutide may aid in guarding against excitotoxic cell damage. The peptide has been hypothesised to promote the development of neurites in cells grown in a lab. Scientists are keeping their fingers crossed that Semaglutide might be the key to stopping or perhaps reversing certain forms of neurodegeneration.

Curiously, research in mice models has hinted that Semaglutide and its counterpart, Exendin-4, may decrease brain amyloid-beta and the beta-amyloid precursor protein in neurons. The major component of the Alzheimer’s disease plaques, which are not directly responsible for the illness but are linked to its severity, is amyloid beta. While the efficacy of this strategy in warding off Alzheimer’s disease is still unknown, it does provide intriguing new information on how researchers may slow the illness’s development from moderate cognitive impairment to full-blown Alzheimer’s.

The Semaglutide for sale available at Core Peptides is strictly for research and educational purposes; it is not meant for human consumption. You must be a licensed researcher to purchase Semaglutide.

Semaglutide peptide and cardiovascular activity

Research has proposed that GLP-1 receptors may be found throughout the heart and may enhance cardiac function in some situations by increasing heart rate and decreasing left ventricular end-diastolic pressure. Although it may not seem significant, elevated left ventricular end-diastolic pressure is linked to left ventricular hypertrophy, cardiac remodelling, and, ultimately, heart failure.

More recent research has even hinted that GLP-1 may help reduce total heart attack damage. The peptide seems to enhance glucose absorption in cardiac muscle, which aids cells in battling ischemia, allows them to continue working, and prevents programmed cell death. It seems that insulin is not necessary for these cells to experience an increase in glucose absorption.

Research in dogs has theorised that reducing systemic vascular resistance and improving LV function may be achieved with large-scale GLP-1 infusions. This second impact may have the potential to lower blood pressure, which in turn reduces cardiac strain. Subsequently, this appears to have the potential to mitigate LV remodelling, vascular thickening, and heart failure, which are long-term effects of hypertension. “Constantly increased myocardial performance in experimental animal models,” says Dr Holst of the effects of giving GLP-1 after heart damage.


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