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GHRP-6

Growth Hormone Releasing Peptide-6, Growth hormone-releasing hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2

Quick Stats
Studies 702
Trials 0
Score 2
2008 pubmed

Association between tumoral GH-releasing peptide receptor type 1a mRNA expression and in vivo response to GH-releasing peptide-6 in ACTH-dependent Cushing's syndrome patients.

Machado. Marcio Carlos MC; Valeria de Sa. Sandra S; Correa-Giannella. Maria Lucia ML; Giorgi. Ricardo Rodrigues RR; Pereira. Maria Adelaide Albergaria MA; Cescato. Valter Angelo S VA; Giannella-Neto. Daniel D; Salgado. Luiz Roberto LR

Key Findings

  • Patients whose tumors expressed more GHSR‑1a mRNA had a larger ACTH and cortisol response to GHRP‑6.
  • Overall GHSR‑1a expression in tumor tissue was similar to normal pituitary tissue, indicating variability among patients.

Practical Outcomes

  • For biohackers, the main takeaway is that GHRP‑6 can provoke cortisol spikes in people with certain pituitary abnormalities, so monitoring adrenal hormones may be wise if you have any undiagnosed endocrine issues. The findings don’t suggest a new dosing strategy for healthy users, but they highlight a potential safety consideration.

Summary

The study examined people with Cushing's disease (a condition with too much cortisol) and found that those whose tumors had higher levels of the GH‑releasing peptide receptor (GHSR‑1a) showed a stronger ACTH and cortisol rise after receiving GHRP‑6. In healthy individuals the peptide is used to boost growth hormone, but this research shows that in certain disease states GHRP‑6 can also stimulate stress hormones, depending on receptor expression.

Abstract

GH secretagogues (GHS) produce exaggerated ACTH and cortisol responses in Cushing's disease (CD) patients, attributable to their direct action on GH-releasing peptide receptor type 1a (GHSR-1a). However, there are no studies correlating the in vivo response to GHS and GHSR-1a mRNA expression in ACTH-dependent Cushing's syndrome (CS) patients. The aim of this study is to correlate the patterns of ACTH and cortisol response to GH-releasing peptide-6 (GHRP-6) to GHSR-1a expression in ACTH-dependent CS patients. Prospective study in a tertiary referral hospital center. Fifteen CD patients and two ectopic ACTH syndrome (EAS) patients were studied. Tumor fragments were submitted to RNA extraction, and GHSR-1a expression was studied through real-time qPCR and compared with normal tissue samples. The patients were also submitted to desmopressin test and vasopressin receptor type 1B (AVPR1B) mRNA analysis by qPCR. GHSR-1a expression was similar in normal pituitary samples and in corticotrophic tumor samples. GHSR-1a expression was higher in patients (CD and EAS) presenting in vivo response to GHRP-6. Higher expression of AVPR1B was observed in the EAS patients responsive to desmopressin, as well as in corticotrophic tumors, as compared with normal pituitary samples, but no correlation between AVPR1B expression and response to desmopressin was observed in the CD patients. Our results revealed a higher expression of GHSR-1a in the ACTH-dependent CS patients responsive to GHRP-6, suggesting an association between receptor gene expression and in vivo response to the secretagogue in both the CD and the EAS patients.

Study Information

Provider

pubmed

Year

2008

DOI

10.1530/eje-07-0659