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GHRP-2

Pralmorelin, Growth Hormone Releasing Peptide-2, KP-102

Quick Stats
Studies 230
Trials 1
Score 4
2009 pubmed

Preservation of GHRH and GH-releasing peptide-2 efficacy in young men with experimentally induced hypogonadism.

Veldhuis. Johannes D JD; Keenan. Daniel M DM; Bailey. Joy N JN; Miles. John M JM; Bowers. Cyril Y CY

Key Findings

  • Short‑term hypogonadism (low testosterone/estradiol) did not blunt the GH‑raising effect of GHRP‑2 or GHRH.
  • GHRP‑2 produced a particularly robust GH response that was independent of visceral fat, IGF‑1, IGFBP‑1, or IGFBP‑3 levels.
  • Low testosterone reduced basal (non‑pulsatile) GH but did not affect pulsatile GH secretion or IGF‑1/IGFBP‑3 concentrations.

Practical Outcomes

  • You can likely include GHRP‑2 in a GH‑boosting protocol without worrying about your current testosterone status or body‑fat levels, making it useful during TRT cycles or low‑testosterone phases. The study only looked at short‑term hormone suppression, so long‑term effects remain unknown, but the data support GHRP‑2 as a reliable GH secretagogue for short‑term use.

Summary

In healthy young men whose testosterone was temporarily knocked down, both GHRH and the peptide GHRP‑2 still caused a strong rise in growth hormone. GHRP‑2 was especially reliable, working no matter how low the sex hormones were, how much belly fat they had, or what their IGF‑1 levels were. This suggests you can use GHRP‑2 to boost GH even when you’re low on testosterone, at least in the short term.

Abstract

Somatostatin (SS), GHRH, GH-releasing peptide (GHRP), and the sex-steroid milieu regulate GH secretion. To test whether GHRH and GHRP remain effective secretagogs in the face of short-term hypogonadism. Prospective, randomized double-blind. Healthy young men (n=24) received a GnRH agonist twice 3 weeks apart followed by placebo (n=13, Pl) or testosterone (n=11, testosterone) addback. were then given consecutive i.v. infusions of l-arginine (to restrain SS outflow) and a maximally effective dose of GHRH or GHRP-2 (to test corresponding secretagog pathways). GH secretion stimulated by l-arginine/GHRH and by l-arginine/GHRP-2 was unaffected by combined testosterone/estradiol (E(2)) depletion. The low testosterone/E(2) milieu decreased basal (nonpulsatile) GH secretion (P=0.038), without altering fasting pulsatile GH secretion or IGF1 or IGF-binding protein (IGFBP)-3 concentrations. IGFBP-1 (P<0.0001) and abdominal visceral fat (AVF, P=0.017) correlated negatively with fasting basal GH secretion. By contrast, IGF1 (P=0.0012) and IGFBP-3 (P=0.015) correlated positively with fasting pulsatile GH secretion. AVF (P=0.0024) was a negative determinant, and IGF1 a positive determinant (P=0.018), of GHRH-driven GH pulses. Responses to GHRP-2 were unrelated to any of these factors. l-arginine/GHRP-2 appears to be an especially robust stimulus of GH secretion, since efficacy is unmodified by profound short-term hypogonadism, a range of AVF estimates, and a spectrum of IGF1, IGFBP-1, and IGFBP-3 concentrations. Whether robustness also applies to chronic hypogonadism is not known.

Study Information

Provider

pubmed

Year

2009

Date

2009-05-20T00:00:00.000Z

DOI

10.1530/eje-09-0270