GHRP 6 is not an active fragment of growth hormone releasing hormone (GHRH). It is one of several synthetic met-enkephalin analogs that include unnatural D-amino acids that were developed for their growth hormone releasing activity and are called growth hormone secretagogues. GHRP 6 is a true hGH secretagogue. Which means it stimulates the body’s own secretion of hGH as explained in the study below. Human Growth hormone has been shown in studies to promote lean body mass and reduce adiposity (fat). It is now known that these growth hormone releasing peptides are distinct from GHRH and do not act at the GHRH receptor, but instead act at the growth hormone secretagogue receptor, now renamed as the ghrelin receptor. It is for this reason (gherlin like properties) patients being treated with GHRP 6 experience appetite stimulation. In therapy GHRP 6 is used to stimulate growth hormone production whilst increasing body mass. Patients deficient in growth hormone and underweight would be ideal candidates for GHRP 6.
Growth hormone releasing peptide (GHRP 6) stimulates phosphatidylinositol (PI) turnover in human pituitary somatotroph cells.
Lei T, Buchfelder M, Fahlbusch R, Adams EF.
Source: Department of Neurosurgery, University of Erlangen-Nürnberg, Germany.
Abstract: Growth hormone releasing peptide (GHRP 6) is a synthetic hexapeptide which specifically stimulates secretion of growth hormone (GH) by pituitary somatotrophs. The precise intracellular mechanism by which this is achieved has not been deciphered although it is known to involve protein kinase C (PKC) and Ca2+ but to be cAMP-independent. We have used cell cultures of human pituitary somatotrophinomas to demonstrate powerful effects of GHRP 6 on membrane phosphatidylinositol (PI) turnover, a second messenger system which leads to activation of PKC and mobilisation of intracellular Ca2+ reserves. Incubation of somatotrophinoma cells with GHRP 6 led to a dose-dependent stimulation of rate of PI turnover. GH secretion was increased in parallel. Effects were discernable after only 15 minutes incubation and rose to a maximum at 2 hours. PI turnover was stimulated by GHRP 6 in 8 of 8 tumours examined, effects ranging from 2.1 – 7.9 fold increases. Stimulation of GH secretion by GHRP 6 was independent of presence of gsp oncogenes, emphasising the cAMP-independent nature of its effects. These results provide evidence that the GH-stimulatory effects of GHRP 6 are achieved through activation of the PI second messenger system and thus support earlier findings that PKC and Ca2+ play central roles in mediating the effects of GHRP 6.
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