GHRP-6
Growth Hormone Releasing Peptide-6, Growth hormone-releasing hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2
Impairment of GH responsiveness to GH-releasing hexapeptide (GHRP-6) in Prader-Willi syndrome.
Grugni. G G; Guzzaloni. G G; Morabito. F F
Key Findings
- GH release after GHRP‑6 is markedly reduced in Prader‑Willi patients versus obese or short normal controls.
- The blunted response is not just due to obesity; it reflects a hypothalamic‑pituitary dysfunction specific to the syndrome.
- Low IGF‑1 levels were present in all Prader‑Willi subjects, and none showed a normal GH response on prior stimulation tests.
Practical Outcomes
- For most biohackers, this study has limited direct use because it focuses on a rare condition. However, it warns that GHRP‑6 may be ineffective in individuals with severe hypothalamic or pituitary defects. If you have known endocrine disorders, especially affecting the GH axis, you might not expect the usual GH‑boosting effects from GHRP‑6.
Summary
The study shows that people with Prader‑Willi syndrome (a rare genetic disorder) have a much weaker growth‑hormone response to the peptide GHRP‑6 compared to obese or short‑stature children without the syndrome. Their GH levels after GHRP‑6 were similar to those after a standard GH‑releasing hormone test, and all had low IGF‑1, indicating a broader pituitary problem.
Abstract
The aim of this study was to evaluate the GH-releasing activity of a synthetic hexapeptide, GHRP-6, in the Prader-Willi syndrome (PWS). Sixteen PWS patients (7 males and 9 females, aged 12.7-38.3 yr), 15 with essential obesity (OB) (7 males and 8 females, aged 12.9-42.9 yr), and 8 short normal children (SN; 3 males and 5 females, aged 10.2-14.3 yr) underwent 2 tests on separate occasions, being challenged with GHRP-6 (1 microg/kg, iv) or GHRH (1 microg/kg, iv)+PD (60 or 120 mg for children or adults, po). Moreover, in 11 patients with PWS and in the group of SN, the GH response to at least 2 stimulation tests had been previously determined. GH was analyzed either as mean peak values (GHp, mcg/l), or as the area under the curve (AUC, mcg/l/h) and the net incremental area under the curve (nAUC, mcg/l/h). In the group of PWS subjects, GH responses to both GHRP-6 (GHp: 11.4+/-2.0; AUC: 588+/-113; nAUC: 483+/-108) and GHRH+PD (GHp: 7.3+/-1.8; AUC: 486+/-122; nAUC: 371+/-250) were significantly lower than those observed either in OB (GHRP-6: GHp: 25.7+/-3.2, p<0.003; AUC: 1833+/-305, p<0.005; nAUC: 1640+/-263, p<0.0001. GHRH+PD: GHp: 15.1+/-2.4, p<0.009; AUC: 1249+/-248, p<0.003; nAUC: 918+/-230, p<0.006) or in SN patients (GHRP-6: GHp: 39.1+/-3.1, p<0.0001; AUC: 2792+/-158, p<0.0001; nAUC: 2705+/-165, p<0.00005. GHRH+PD: GHp: 27.5+/-3.7, p<0.0001; AUC: 1873+/-251, p<0.0001; nAUC: 1692+/-219, p<0.0005). Unlike control groups, in PWS patients GH levels after GHRP-6 did not differ from those obtained after GHRH+PD. Interestingly, low IGF-I values were present in all PWS subjects. Furthermore, no patient with PWS showed normal GH response to the previously performed GH stimulation tests. As already reported, GH release after GHRP-6 or GHRH+PD was significantly lower in OB than in SN subjects. In conclusion, our data indicate that: 1) GH response to GHRP-6 is clearly impaired in PWS; 2) the blunted GH responses to the provocative stimuli in PWS are not an artifact of obesity; 3) short stature in PWS is caused by a complex dysfunction of the hypothalamo-pituitary structures.
Study Information
pubmed
2001
10.1007/bf03343871