Liraglutide (GLP-1) (3mg)

Liraglutide (GLP-1) Peptide

Liraglutide is a chemical peptide, which belongs to the class of glucagon-like peptide-1 receptor agonists (GLP-1RAs). It mimics the GLP-1 peptide hormone that occurs naturally, containing 31 amino acids in its active form. Specifically, Liraglutide appears to exert a 97% similarity to the active form of GLP-1. It appears to function primarily in lowering blood glucose levels through activation on beta cells of the Islet of Langerhans to produce insulin. Its apparent functions may not be limited to blood glucose reduction, it may also act on the gastrointestinal tract (GIT), cardiovascular system, and brain. It has also been researched for potential function within fat tissues, muscle tissues, bone, liver, lungs, and kidneys.

Liraglutide Peptide and the Brain

Studies have suggested that Liraglutide (GLP-1) peptides may improve cognitive function and protect brain neurons against neurodegeneration such as in Alzheimer’s disease models through mitigation of amyloid-beta accumulation.[5] Its precise mechanism of action requires further research. Amyloid beta is considered to be the primary component found in Alzheimer’s disease that is associated with its severity.[6

Liraglutide Peptide and the Cardiovascular System

Researchers have hypothesized that Liraglutide may be distributed evenly across the heart, appearing to improve cardiac function by reducing the left ventricular end-diastolic pressure, and boosting the heart rate.[7] The researchers note that

“The defective cardiovascular response to insulin was not attributable to a generalized defect in the stress response, because GLP-1R(-/-) mice responded appropriately to insulin with increased c-fos expression in the hypothalamus and increased circulating levels of glucagon and epinephrine.”

Increased LV end-diastolic pressure is one of the considered causes of LV hypertrophy, cardiac remodeling, and eventual heart failure. Thus, Liraglutide may function to mitigate these cases. Researchers further suggest that Liraglutide may improve the uptake of glucose by cardiac muscles, thus supporting cardiac muscles under the struggle of ischemia facilitate nutritional absorption to aid continuous function and avoid apoptosis. According to the research by Dr. Holst, the continuous exposure of GLP-1 receptor agonists like Liraglutude following a cardiac injury may “constantly increase myocardial performance in […] experimental models.

Liraglutide Peptide and Beta-Cell Protection

In this research study, animal models were used to extrapolate possible impacts of Liraglutide on pancreatic beta cells.[8] Here, Liraglutide was reported to apparently accelerate the growth and proliferation of pancreatic beta cells. Researchers also suggested that GLP-1 receptor agonists like Liraglutide may have increased the differentiation of new beta cells from beta-cell progenitors in the epithelium of the pancreatic duct. This reported impact elicited by the Liraglutide peptide has suggested a potential in diabetes-related research. In one of the studies, Liraglutide appeared to halt the death of beta cells caused by increased levels of inflammatory cytokines. In another experimental mouse model, where the mice had type 1 diabetes, Liraglutide appeared to protect the cells of the Islets of Langerhans from death.

Liraglutide Peptide and Adipose Cells

Adipose tissue, known for storing energy and producing various hormones, might be influenced by Liraglutide’s mechanisms, which might impact hormones such as leptin and peptide YY (PYY) that are believed to be involved in energy regulation and satiety.[9] Leptin, primarily produced by fat cells (adipocytes), is thought to communicate with the central nervous system to influence food intake and energy expenditure. In most cases, rapid weight loss typically leads to a reduction in leptin levels, which may increase appetite and lower metabolic rate. Liraglutide might help sustain weight loss by potentially mitigating the drop in leptin levels that usually accompanies weight reduction.

Peptide YY (PYY) is a hormone that is believed to be secreted by the gut following food intake, and it may contribute to satiety and reduced appetite. Some studies suggest that Liraglutide might raise PYY levels, which may upregulate its potential appetite-suppressing actions. This interaction might explain the reduced energy intake and weight loss observed in some experimental settings involving Liraglutide. Additionally, Liraglutide may have the capacity to improve the function of adipocytes, which might lead to a more favorable metabolic profile. This improvement might involve changes in adipokine levels—hormones produced by adipose tissue—that might upregulate insulin sensitivity and potentially reduce inflammation associated with obesity models. However, these mechanisms remain to be fully understood and require further investigation.

Liraglutide Peptide and Gastrointestinal Tissues

Liraglutide appears to activate GLP-1 receptors (GLP-1Rs) located on enteroendocrine cells within the gut.[10] These enteroendocrine cells are generally understood to play a role in responding to food intake by secreting GLP-1, a hormone involved in various gastrointestinal processes. Liraglutide may mimic these natural actions by engaging the GLP-1Rs. When Liraglutide activates these receptors, it is believed that signaling occurs through the enteric nervous system, which controls the motility of the gastrointestinal tract. This receptor engagement is hypothesized to influence neural pathways that regulate the rate of gastric contractions and the progression of contents through the digestive system, potentially leading to a decrease in gastric motility and a consequent delay in gastric emptying.

Additionally, Liraglutide’s activation of GLP-1 receptors might initiate signaling through the vagal nerve, which communicates with the central nervous system (CNS). This interaction might further modulate the autonomic nervous system’s regulation of gastric motility, possibly reinforcing the deceleration of gastric emptying. This suggests that Liraglutide may slow down gastric emptying via a complex mechanism, potentially involving the interplay between neural circuits that include GLP-1 receptors in both the CNS and peripheral nervous system.

Experimental observations in laboratory models indicate that Liraglutide may reduce gastric emptying by approximately 23% within the first hour after exposure, compared to a placebo. However, this initial delay does not appear to extend to the overall gastric emptying over a 5-hour period, as measured by the area under the curve (AUC0–300 min). This short-term reduction in gastric motility might, however, be sufficient to promote an early sense of satiety.[11]

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