Liraglutide (GLP-1) (3mg)

Liraglutide (GLP-1) Peptide

Liraglutide (GLP-1) is a chemical peptide, known also as Glucagon Like Peptide-1 (GLP-1). It is a peptide hormone that occurs naturally, containing roughly 30 to 31 amino acids. 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.

Specifications

Molecular Formula: C₁₇₂H₂₆₅N₄₃O₅₁

Molecular Weight: 3751.20 g/mol

Synonyms: GLP-1, proglucagon (72-108), Glucagon – peptide – 1, victoza, Liraglutida, Liraglutidum, NN2211

Liraglutide Research

Liraglutide Peptide and Incretin
According to research by Dr. Holst on GLP-1, the most critical potential of the Liraglutide is its proposed “Incretin Effect”.^[1] The researcher explains that “The main actions of GLP-1 are to stimulate insulin secretion (i.e., to act as an incretin hormone) and to inhibit glucagon secretion, thereby contributing to limit postprandial glucose excursions.” Incretin is a collection of hormones that appear to function to decrease blood glucose levels. These hormones are the glucose-dependent insulinotropic polypeptide (GIP) and the glucagon-like peptide (GLP-1). According to this research, Liraglutide may potentially be classified among the incretin hormones, and may serve as a potent member of the incretin family, particularly, researchers suggest, in conditions of severe hyperglycemia.^[2] Traces of the Liraglutide have been reported to be found on the surface of the pancreatic beta cells (insulin producers). Thus, Liraglutide (GLP-1) may have the potential to directly accelerate insulin production from the pancreas. In cases where the Liraglutide was studied in combination with Sulfonylurea compounds, it appeared to accelerate insulin production to the extent where it may have induced hypoglycemia, as seen in some research models.^[3] Research results have been varied. Increased insulin in the blood is often associated with increased protein synthesis, increased uptake of amino acids by skeletal muscle, and the reduction in the breakdown of protein.

Liraglutide Peptide and Hunger Hormone Signaling
Studies on mouse models exposed to Liraglutide (GLP-1) have been used to develop experimental theses on the impact of the peptide within the brain.^[4] The peptide appeared to reduce the drive to eat via hormone signaling to the brain, inhibiting hunger indirectly. The mouse models exposure to the peptide appeared to lead to gradual and linear weight loss. Introduction of Liraglutide over a long period eventually appeared to exhibit a reduction in hemoglobin A1C levels, which is suggested to be a proxy marker for severe diabetes. Exposure over a long period was also suggested to lead to possible improvement in cardiovascular risk factors. A reduction in hemoglobin A1C levels, indicating severe diabetes, appears to be mitigated with quality control of the blood glucose level.

Liraglutide Peptide and the Brain
Studies have suggested that Liraglutide (GLP-1) peptides may improve cognitive function and protect brain neurons against neurodegenerative diseases such as Alzheimer’s disease 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. It is not known to be a causative agent yet, but it is associated with the severity of the disease. Researchers are still finding out if preventing the accumulation of amyloid-beta can protect hosts against Alzheimer’s.^[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 Liraglutude (GLP-1) 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 Liraglutide (GLP-1) 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.

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