Hexarelin is classified as a synthetic growth hormone-releasing peptide (GHRP) that has been widely studied within the context of cardioprotection and cell function. This peptide has been employed in laboratory conditions to elucidate the action of ghrelin, a hormone which requires acylation to bind to GHS-R1a and consists of 28 amino acids. Hexarelin gets part of its name from hexapeptide, as the peptide is made of 6 amino acids. The other part of its name is derived from the synthetic analog of ghrelin. Hexa(six) and (gh)relin, hexarelin.
Autophagy management is considered a contributor to cardioprotection. One study investigated the function of potential governing mechanisms and autophagy and suggested that heart muscle cells’ hypertrophy, cell death, and oxidative stress were reportedly inhibited by Hexarelin exposure. Hexarelin peptide appeared to manage the upward autophagy signaling by slowing the mTOR phosphorylation. Researchers of this study proposed that Hexarelin may reduce hypertrophy of heart muscle cells and cell death.
Hexarelin is researched primarily within the context of the pituitary gland, and studies have suggested it may also induce additional endogenous production of growth hormone. Similar to its growth hormone-releasing peptide counterparts, it may potentially act to inhibit somatostatin functions while elevating growth hormone levels through magnifying the GHRH signal transduction pathway.
Hexarelin Peptide Structure, Weight
Hexarelin has a molecular structure of C47H58N12O6 and a molecular weight of 887 grams per mole. Its sequence is His-D-2-methyl-Trp-Ala-Trp-D-Phe-Lys-NH2, and it has a chemical abstract service (CAS) registry of 140703-51-1.(1)
Hexarelin Mechanism of Action
Hexarelin peptide appears to function using receptors at both the hypothalamic and pituitary levels to potentially promote growth hormone discharge, as suggested by findings in animal model research. Researchers hypothesize that the release of growth hormone using PKC signaling may be affected by Hexarelin. It may potentially copy ghrelin function by attaching to GHS-R1a, and scientists consider that it may also attach to and fire up cardiac receptors.
Hexarelin appears to enact adrenocorticotropin and prolactin cortisol-releasing activity, which is considered similar to other growth hormone releasing peptides. Thyroid-stimulating hormone, luteinizing hormone, IGF-1, follicle-stimulating hormone, and plasma glucose are all reportedly unaffected by the exposure of Hexarelin.
Hexarelin and Other GHRPs
Upon data examination, Hexarelin appears to contain unique aspects absent in other GHRPs. On a microgram to microgram level comparison, Hexarelin has been reported to exceed the other growth hormone releasing peptides in action, as observed in contained laboratory conditions. Though it requires further scientific investigation, initial studies report an increased, accelerated desensitization rate as opposed to other research peptides, but the rate and extent of this are still being studied.
Hexarelin has presented the potential for joint restoration, protection, and healing, neural protection, muscle fiber size increase, and enhanced strength when introduced to animal models in research studies. The peptide is also suggested to decrease overall fatty tissue, though this must be further substantiated by ongoing research. Any form of growth within an organism is considered solely a result of the rise in hormone levels; gastric draining does not appear to be accelerated, and appetite is not stimulated.
Research
Researchers generally cease Hexarelin exposure within 2 weeks of initial introduction, as seen on average within the body of research on animal models. Doing otherwise was reported in some studies to potentially lead to an insignificant rise in growth hormone production due to, potentially, an increase in desensitization. A study opposing this practice was conducted. The experiment was performed on animal research subjects to examine Hexarelin’s desensitization rate in daily exposure. The subjects’ blood was drawn four times over 16 weeks and analyzed. Upon evaluation, the researchers concluded that Hexarelin appeared to have presented an insignificant difference in desensitization after the first and fourth week of exposure.
Animal subjects exposed to Hexarelin reportedly presented muscle size increases, likely resulting from new myocytogenesis. Hexarelin also displayed accelerated injury recovery and, in some cases, was observed to have benefited cardiac functioning. Animal subjects without the ability to generate their own hGH naturally, were observed over the course of the study. The peptide has also been researched for its potential to increase epidermal elasticity, and has been suggested by researchers to exhibit properties that encompass possible injury prevention through increased epidermal structure and strength, and hastened recovery in damaged tissue.
Hexarelin has been suggested to provide a variety of properties, with its most prominent potential actions speculated within the realm of fat regulation, cardiac protection, and muscle mass preservation.
Initial research supports Hexarelin’s potential as a CD36 agonist, a protein involved in lipolysis control, and management of fatty acid breakdown. Exposure of cultured murine adipose to Hexarelin reportedly resulted in CD36 activation, which scientists reported drew out the reduced expression of PEPCK.(2) Since PEPCK is linked to the breakdown of fatty acids, this implies that this process may be regulated by CD36, and may potentially be thus activated by this peptide.
Abnormal amounts of fat in the blood are referred to as dyslipidemia. Rodent research suggests that growth hormone-releasing peptide 6 (GHRP-6) may potentially inhibit dyslipidemia in an insulin resistance setting while lowering blood sugar and insulin resistance. Hexarelin may potentially provide an alternative to the lipid compounds currently widespread in research studies within the context of severe dyslipidemia.
Hexarelin Research in Cardiovascular Function
Researchers suggest Hexraelin may be linked to positive effects on cardiac tissues, especially in instances of disease or injury. Study results support Hexarelin’s potential ability to relieve lesion formation in rodent atherosclerosis models. Hexarelin appears to affect the heart directly by attaching to the CD36 receptor and the GHSR. Rodent studies suggest that the peptide may potentially guard cardiac cells against heart attack by attaching to these receptors and inhibiting cells from going through programmed cell death (aka apoptosis). Hexamorelin-exposed rodents reportedly presented a higher number of surviving cardiac cells, reduced formation of malondialdehyde (an indicator of heart cell death), and apparently increased cardiac function compared to controls.
Another study suggested that Hexarelin appeared to decrease oxidative stress in cardiac failure and inhibit remodeling of heart muscles from occurring. Remodeling is a process having to do with a decrease in cardiac function and morbidity.(3) GHRP 6-exposed rodents in this study exhibited apparent enhancements in cardiac function. The processes are considered to be arbitrated by Hexarelin/GHRP 6 down-regulation of protein kinase B expression and up-regulation of PTEN activity.
Since the mechanism that Hexarelin potentially employes which supposedly protect cardiac cells is not particular to the damage mechanism in myocardial infarctions, scientists suppose that Hexarelin may be researched further with the context of cardiac protection and other injuries. A study on rodents reported that the peptide appeared to enhance cardiac function in a diabetes model by manipulating the way potassium and calcium are processed by myocardial cells.
Hexarelin Peptide and Muscle Mass
Hexarelin may potentially provoke a rise in calcium influx by activating the GHS-R1a, though it did not appear to induce this impact on skeletal muscle. Hexarelin has been reported by researchers to host an ability to improve isolated skeletal muscle contractility of rats in a way that is significantly calcium-independent and concentration-dependent.
Rodent studies of cachexia models have suggested that Hexarelin may protect myocytes through managing calcium flow and mitochondrial dysfunction. Mitochondria are the power plants of cells. Without them, cells can’t generate the energy necessary to perform normal function and will die eventually.
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References:
- National Center for Biotechnology Information. PubChem Database. Examorelin CID 6918297. 2020.
- Ma Y, et al. Growth hormone secretagogues protect mouse cardiomyocytes from in vitro ischemia/reperfusion injury through regulation of intracellular calcium. PLoS One Journal, 2012.
- Wan Z, et al. FAT/CD36 regulates PEPCK expression in adipose tissue. American journal of physiology. Cell physiology, 2013.