GHRP-6
Growth Hormone Releasing Peptide-6, Growth hormone-releasing hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2
Effects of ghrelin, GH-releasing peptide-6 (GHRP-6) and GHRH on GH, ACTH and cortisol release in hyperthyroidism before and after treatment.
Molica. Patricia P; Nascif. Sergio Oliva SO; Correa-Silva. Silvia Regina SR; de Sá. Larissa Bianca Paiva Cunha LB; Vieira. José Gilberto Henriques JG; Lengyel. Ana-Maria Judith AM
Key Findings
- GH spikes after ghrelin, GHRP‑6, and GHRH are markedly lower in untreated hyperthyroid patients compared to normal controls.
- After thyroid treatment, GH responses improve in about half the patients but remain below control levels.
- ACTH response to ghrelin is roughly double in hyperthyroid patients before treatment, showing a trend toward reduction after thyroid normalization.
- Cortisol responses to ghrelin and GHRP‑6 are similar to controls and do not change with thyroid treatment.
Practical Outcomes
- If you plan to use GHRP‑6 for GH boosting, make sure your thyroid function is normal first, as excess thyroid hormone can blunt the GH effect. Expect that correcting hyperthyroidism may only partially restore the GH response, so other factors (dose, timing, nutrition) will still matter. The study does not suggest any new dosing regimen, but highlights the importance of thyroid health for optimal peptide performance.
Summary
In people with an overactive thyroid, the body’s growth‑hormone (GH) response to GHRP‑6 and other GH‑releasing peptides is weaker than in healthy folks, and even after the thyroid is fixed the response doesn’t fully bounce back for many. The stress‑hormone (ACTH) reaction to ghrelin is higher when the thyroid is overactive, but cortisol levels stay about the same.
Abstract
In thyrotoxicosis GH responses to stimuli are diminished and the hypothalamic-pituitary-adrenal axis is hyperactive. There are no data on ghrelin or GHRP-6-induced GH, ACTH and cortisol release in treated hyperthyroidism. We, therefore, evaluated these responses in 10 thyrotoxic patients before treatment and in 7 of them after treatment. GHRH-induced GH release was also studied. Peak GH (μg/L; mean ± SE) values after ghrelin (22.6 ± 3.9), GHRP-6 (13.8 ± 2.3) and GHRH (4.9 ± 0.9) were lower in hyperthyroidism before treatment compared to controls (ghrelin: 67.6 ± 19.3; GHRP-6: 25.4 ± 2.7; GHRH: 12.2 ± 2.8) and did not change after 6 months of euthyroidism (ghrelin: 32.7 ± 4.7; GHRP-6: 15.6 ± 3.6; GHRH: 7.4 ± 2.3), although GH responses to all peptides increased in ~50% of the patients. In thyrotoxicosis before treatment ACTH response to ghrelin was two fold higher (107.4 ± 26.3) than those of controls (54.9 ± 10.3), although not significantly. ACTH response to GHRP-6 was similar in both groups (hyperthyroid: 44.7 ± 9.0; controls: 31.3 ± 7.9). There was a trend to a decreased ACTH response to ghrelin after 3 months of euthyroidism (35.6 ± 5.3; P = 0.052), but after 6 months this decrease was non-significant (50.7 ± 14.0). After 3 months ACTH response to GHRP-6 decreased significantly (20.4 ± 4.2), with no further changes. In hyperthyroidism before treatment, peak cortisol (μg/dL) responses to ghrelin (18.2 ± 1.2) and GHRP-6 (15.9 ± 1.4) were comparable to controls (ghrelin: 16.4 ± 1.6; GHRP-6: 13.5 ± 0.9) and no changes were seen after treatment. Our results suggest that the pathways of GH release after ghrelin/GHRP-6 and GHRH are similarly affected by thyroid hormone excess and hypothalamic mechanisms of ACTH release modulated by ghrelin/GHSs may be activated in this situation.
Study Information
pubmed
2010
2010-07-03T00:00:00.000Z
10.1007/s11102-010-0238-3
8
56