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Note: NaCl and Bacteriostatic Water are now sold separately.
Summarized research in applications of GHRP-2:
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.
BMI and age also play a role in the efficacy of GHRP-2 although studies note that BMI is a lessor factor in those who are hypogonadal.
In eugonadal men, peak GH concentrations correlated negatively with BMI. In particular, BMI accounted for only 38% of the response variability after L-arginine/GHRH (P=0.0165), but 62% after GHRH/GHRP-2 (P=0.0012) and 65% after L-arginine/GHRP-2 (P=0.00075). In contrast, in hypogonadal men, GH responses were uncorrelated with BMI. The negative effects of BMI on peak GH responses in eugonadal and hypogonadal states differed most markedly after stimulation with GHRH/GHRP-2 (P=0.0019). This contrast was corroborated using integrated GH responses (P=0.0007).
Now, having said that, this still works very well in stimulating GH production. It has a short half life with peak concentrations occurring around 15 minutes and not longer than 60 minutes after administration.
The influences of age, gender and adiposity on GH response to GHRP-2 were analysed for all 77 control
subjects and the results are shown in Table 2. There were no significant differences in GH Cmax between males and
females in the age range 20-59 years, and between preand post-menopausal females in the age range 40-59
years. A small differences in the Cmax of serum GH was observed between males and females aged over 60 years
(PZ0.030). Among the three age groups assessed, significant differences were observed; the GH Cmax was
higher in the age group of 2039 years than in the age group of 40-59 years (P0.001) and over 60 years
(P0.001). A significant difference was also observed between overweight (BMIR25 kg/m2 and 30 kg/m2;
P0.001) or obese (BMIR30 kg/m2; PZ0.019) subjects and lean (BMI25 kg/m2) subjects in the age group
20-39 years. In the age group O40 years, BMI affected the Cmax of serum GH even within lean (BMI25 kg/m2)