GHRP – 2 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). ‘The group compared ITT to stimulation with GH releasing
peptide 2 (GHRP-2). The synthetic hexapeptide, also named pralmorelin,
is derived from a metenkephalin peptide. It is the most potent
of the family of synthetic GH stimuli known in humans and acts
via the endogenous ghrelin receptor (12). As these receptors have
been identified both in the hypothalamus and the pituitary, GHRP-2
action may not be restricted to the pituitary. Previous data confirmed
by the recent work of Chihara et al. in the present issue suggest
a dose-dependent and specific GH release in healthy volunteers
independent of age, sex and obesity (13), and support the results
of the combination tests of GHRP-2 with GHRH (14).’ GHRP
– 2 also has a protective effect on the liver and an anti-inflammatory
effect. These are paramount attributes for experiments involving
muscle synthesis and recovery. ‘It has been reported that
growth hormone (GH)-releasing peptide-2 (GHRP-2), a ghrelin receptor
agonist, has an anti-inflammatory effect. We investigated whether
this GH secretagogue attenuates liver injury in LPS-treated rats.
Wistar rats were simultaneously injected (ip) with LPS (1 mg/kg)
and/or GHRP-2 (100 microg/kg). Serum
levels of aspartate and alanine transaminases were measured as
an index of liver damage. Circulating nitrites/nitrates and hepatic
IGF-I and TNF-alpha were evaluated as possible mediators of GHRP-2
actions. LPS increased serum levels of transaminases and nitrites/nitrates.
Moreover, LPS increased hepatic TNF-alpha and decreased hepatic
IGF-I mRNAs. GHRP-2 administration attenuated the effects of LPS
on transaminases, nitrites/nitrates, TNF-alpha, and IGF-I in vivo.
This GHRP-2 effect does not seem to be due to modifications in
food intake, since fasting did not modify serum levels of transaminases,
serum nitrites/nitrates, and hepatic TNF-alpha mRNA both in vehicle
rats and in LPS-injected rats. To elucidate whether GHRP-2 is
acting directly on the liver, cocultures of hepatocytes and nonparenchymal
cells and monocultures of isolated hepatocytes were incubated
with LPS and GHRP-2. The ghrelin receptor agonist prevented an
endotoxin-induced increase in transaminases and nitrite/nitrate
release as well as in TNF-alpha mRNA and increased IGF-I mRNA
from cocultures of hepatocytes and nonparenchymal cells, but not
from monocultures. In summary, these data indicate that GHRP-2
has a protective effect on the liver in LPS-injected rats that
seems to be mediated by IGF-I, TNF-alpha, and nitric oxide. Our
data also suggest that the anti-inflammatory effect of GHRP-2
in the liver is exerted on nonparenchymal cells.’ GHRP 2
has demonstrated that it is very effective at stimulating GH production
in test subjects. It has a short half life with peak concentrations
occurring around 15 minutes and not longer than 60 minutes after
administration. Effective dosages in humans range from 100mcg
to 3mcg/Kg of body weight and shows to be equally effective in
both men and women.
