GHRP-6 is one of a set of met-enkephalin analogs that are made up of unnatural D-amino acids. These were developed for their potential, in controlling the release of growth hormone, in an animal’s body. These chemicals do not have an opioid component but instead act as a secreagogue in the body.
It has been discovered that you can use GHRP-6 and insulin simultaneously in animals to increase the response of growth hormone to these chemicals. This will increase the processing of dietary fats and carbohydrates as well as increasing the release of growth hormone secretagogues in animals, such as mice. Mice have also been found to see an increase in muscle growth, body composition, memory, cardiac function and glucose metabolism when they are exposed to GHRP-6.
Comparing Gastroprokinetic Effects
To compare the effects of gastroprokinetic of ghrelin, GHRP6 and motailin was administered in vitro and in vivo.
GHRP-6, ghrelin and motilin were injected to the gastric emptying area after intragastric application of Evans blue. The effects of these chemicals were studied using electrical field stimulation.
This study revealed that GHRP-6 and ghrelin accelerated gastric emptying in rats, though motilin did not. Ghrelin was more potent than GHRP-6 but the application response relationship was more bell shaped for ghrelin.
The concentration response curves displayed on muscle strips showed an increase in cholinergic off-concentrations while the ghrelin antagonists were found to reduce on-relaxations on fundic strips.
No effects were seen when motilin was applied in low concentrations. The presence of L-NAME confirmed that ghrelin antagonists could impact motor responses.
Stimulating Food intake and Growth Hormone Secretion
Ghrelin has been identified as an endogenous ligand that reacts with the growth hormone secretagogue receptor that has now been found to display intraperitoneal and intraerecroventricular administration of ghrelin in rats, with stimulated food intake.
Increased feeding was administered rapidly after an ICV administration of the chemicals for 24 hours. Following this administration 3nmol of ghrelin would be given during the magnitude of this feeding stimulation. This was designed to be similar to the NPY.
Plasma growth hormone concentrations following the ICV administration of ghrelin increased.
The rats saw an increase of adrenocorticotrophic hormone, which stimulated thyroid stimulating hormone in turn. This was inhibited following ghrelin administrations. This data suggests that it is possible to identify endogenous hypothalamic peptides and ghrelin in stimulation feedings for growth hormone secretions.
Stimulating Eating without Affecting Plasma Growth Hormone
A study was performed to compare the effects of intracerebroventricular injections of an opiod related hexapeptide to GHRP-6, on stimulating rats to correlate their feeding behavior– with peripheral plasma growth hormone responses.
GHRP-6 was dissolved in a saline solution and injected into the lateral ventricles of adult male rats. An hour after this injection eating patterns was noted and arterial blood specimens were taken at even intervals.
Plasma was assayed for growth hormone. A statistically significant relationship to GHRP-6 applications was found in the instances of eating.
The change from the baseline of plasma growth hormone levels 60 minutes past the application did not appear to be related to this application. It has been concluded that these results in rats suggest that GHRP-6 can be used to stimulate eating, by a mechanism that is independent of properties that are related to growth hormone.
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The growth hormone secretagogues are different from rHGH chemicals because endogenous GH has all five isoforms of the growth hormone while the exogenous only has 20 kilodalton isofroms.
These are secreted from the tissue in different ways and can cause a different administration of growth hormone secretagogues and a different growth hormone pulse rate in the pituitary gland in the animal. In this case growth hormone is also cleared from the body in a few hours without increasing plasma IGF1 levels.