GHRP-6
Growth Hormone Releasing Peptide-6, Growth hormone-releasing hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2
Ghrelin and GHRP-6-induced ACTH and cortisol release in thyrotoxicosis.
Nascif. Sergio Oliva SO; Molica. Patrícia P; Correa-Silva. Silvia Regina SR; Silva. Marcos Roberto MR; Lengyel. Ana-Maria Judith AM
Key Findings
- Hyperthyroid patients have higher basal cortisol (10.7 µg/dL) and ACTH (21.5 pg/mL) than controls.
- Ghrelin caused a significantly larger ACTH increase (ΔAUC 4,189 pg·min/mL) in hyperthyroid subjects versus controls (ΔAUC 1,499).
- Cortisol responses to ghrelin and GHRP‑6 were similar between hyperthyroid patients and healthy controls.
Practical Outcomes
- For most biohackers, the study doesn’t change how you’d normally use GHRP‑6, since the effect was only seen in people with thyroid disease. It does highlight that thyroid status can influence how ghrelin‑like peptides affect the stress axis, so monitoring thyroid health may be wise if you’re combining these peptides with other hormonal interventions.
Summary
In people with an overactive thyroid, their baseline stress hormones (cortisol and ACTH) are already higher. When given ghrelin or the peptide GHRP‑6, the thyroid‑overactive group showed a bigger jump in ACTH (especially with ghrelin) compared to healthy people, but their cortisol rise was about the same. This suggests that excess thyroid hormone makes the body’s ACTH response to ghrelin‑type signals stronger, while the adrenal glands can still keep up with cortisol production.
Abstract
Thyrotoxicosis might alter the hypothalamic-pituitary-adrenal (HPA) axis. We evaluated the effects of ghrelin and GHRP-6 on the HPA axis in 20 hyperthyroid patients and in 9 controls. Mean basal cortisol (microg/dl) and ACTH (pg/ml) levels were higher in hyperthyroidism (cortisol: 10.7 +/- 0.7; ACTH: 21.5 +/- 2.9) compared to controls (cortisol: 8.1 +/- 0.7; ACTH: 13.5 +/- 1.8). In thyrotoxicosis Delta AUC cortisol values (microg/dl.90 min) after ghrelin (484 +/- 80) and GHRP-6 (115 +/- 63) were similar to controls (ghrelin: 524 +/- 107; GHRP-6: 192 +/- 73). A significant increase in Delta AUC ACTH (pg/ml x 90 min) after ghrelin was observed in thyrotoxicosis (4,189 +/- 1,202) compared to controls (1,499 +/- 338). Delta AUC ACTH values after GHRP-6 were also higher, although not significantly (patients: 927 +/- 330; controls: 539 +/- 237). In summary, our results suggest that ghrelin-mediated pathways of ACTH release might be activated by thyroid hormone excess, but adrenocortical reserve is maintained.
Study Information
pubmed
2009
2009-04-26T00:00:00.000Z
10.1007/s11102-009-0181-3
8
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