What Is GLP-1?

Semaglutide or GLP-1 is a naturally occurring peptide known to lower blood sugar levels by modulating insulin production and release.

It is a 30-31 amino acid sequence short peptide. GLP-1 has been proven to affect metabolism and other body systems. These systems include the brain and the heart.

The primary function of Semaglutide (GLP-1) is to regulate blood sugar levels by enhancing insulin secretion. Semaglutide has been investigated for its anti-diabetic properties because it can protect the beta cells of the pancreas from burnout.

GLP-1 upregulates the transcription of the insulin genes and therefore prevents a pathological rise in blood sugar levels by protecting insulin stores.

Although the primary research surrounding Semaglutide is based on its anti-diabetic properties, newer studies are reviewing its role in other dimensions.

Semaglutide or GLP-1 has been linked with neurotrophic effects in the brain and central nervous system. GLP-1 significantly decreases appetite in the GI system by delaying gastric emptying and reducing intestinal motility. Preliminary research has shown the impacts of GLP-1 on the heart, fat, muscles, bones, liver, lungs, and kidneys. The main focus of GLP-1 research has been diabetes treatment/prevention and appetite inhibition, and subsequent investigations focus on the possible cardiovascular advantages of the peptide. More prevalent and thus less robust research focuses on the ability of GLP-1 to stave off neurodegenerative disease. Though this latter area of research is the most recent, it is also the quick-growing domain of GLP-1 investigations now that the peptide has been proved to slow or prevent the accumulation of amyloid-beta plaques in the setting of Alzheimer’s disease.

Blood Sugar Regulation By GLP-1 – The Incretin Effect

One of the most important ways Semaglutide causes a drop in blood sugar levels is by the “incretin effect.” Incretins are hormones released by the gastrointestinal tract. These hormones are secreted in response to high glucose levels in the blood and act to bring down its levels.

The two most important regulators for incretin release are GLP-1. Even though the circulatory levels of the other regulator, i.e., GIP, are higher than that of GLP-1, Semaglutide still is more potent out of the two, particularly in conditions of very high blood sugar levels. Dr. Holst has studied this effect and the link between GLP-1 and incretin and its potency in rodent models.

A GLP-1 receptor has been seen on the surface of pancreatic beta cells, revealing that GLP-1 enhances the exocytosis of insulin from the pancreas. When mixed with sulfonylurea drugs, GLP-1 boosts insulin secretion. It is enough to cause mild hypoglycemia in up to 40% of subjects. Moreover, increased insulin secretion is associated with several trophic results, such as better protein synthesis, a decrease in the breakdown of protein, and enhanced uptake of amino acids by skeletal muscle.

GLP-1 And The Brain

Secondary research on GLP-1 says it might have a neuroprotective role in the CNS and the brain. Administration of Semaglutide can improve cognitive function and protect against certain neurodegenerative diseases like Alzheimer’s disease. This effect was observed when the use of Semaglutide in mice with specific genetic defects caused an improvement in their learning deficit as well as enhanced their associative and spatial learning.

GLP-1 and its analogs have been shown to reduce amyloid-beta deposition in the brain and the beta-amyloid precursor protein found in the neurons. Since the deposition of these beta-amyloid plaques in brain tissue is the primary pathology resulting in Alzheimer’s disease, Semaglutide can play a specific role in protecting the brain from this disease.

Appetite Suppression By Semaglutide

Investigations in mice models reveal that administration of GLP-1, and its similar cousin GLP-1, into the brains of lab animals can reduce the drive to eat and inhibit food intake. GLP-1 may enhance feelings of satiety, helping individuals feel fuller and indirectly reducing hunger. Recent clinical trials have shown in mice that twice-daily administration of GLP-1 receptor agonists causes gradual linear weight loss. Over an extended period, this weight loss is associated with significant improvement in cardiovascular risk factors and reduced hemoglobin A1C levels. The latter is a proxy marker for the severity of diabetes, and the quality of blood sugar control attained via treatment. The effects of this peptide on insulin regulation and appetite suppression can lead to significant weight loss.

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