Plasma neurotensin levels in prepubertal children and adults: possible involvement in the regulation of growth hormone secretion.
Bozzola. M M; Thome. A N AN; Giraldi. E E; Lhiaubet. A M AM; Schimpff. R M RM
Key Findings
- Prepubertal children with growth delay showed significantly higher basal plasma NT levels than normal adults.
- During GH stimulation, NT concentrations fell when GH peaked and rose again as GH levels declined.
- The pattern hints that NT could influence GH secretion indirectly, likely through modulation of somatostatin release.
Practical Outcomes
- For biohackers using GH‑secretagogues like hexarelin, the data imply that neurotensin levels might affect how well these compounds boost GH. While the study doesn’t provide a direct dosing protocol, it suggests that strategies which lower NT (or its upstream triggers) could potentially enhance GH spikes. More research is needed before any concrete recommendations can be made.
Summary
The study found that kids with growth delay have higher blood levels of neurotensin (NT) than adults, and that NT levels dip when growth hormone (GH) spikes after a stimulation test, then rise again as GH falls. This suggests NT might act as a peripheral signal that helps control GH release, possibly by affecting somatostatin.
Abstract
The present study investigated a possible relationship between plasma neurotensin (NT) and serum growth hormone (GH) levels after GH-stimulation provocative tests in humans. Samples were obtained from twelve prepubertal children and sixteen normal adult volunteers. Basal plasma NT levels were higher in children with growth delay (19.02 +/- 4.01 fmol/ml) (mean +/- SEM) than in normal adults (6.13 +/- 1.1 fmol/ml) (p < 0.001). Basal GH levels in children (1.52 +/- 0.06 ng/ml) were not different from those in adults (0.60 +/- 0.41 ng/ml). After stimulation of GH secretion, NT values decreased when GH peaked, and increased when GH levels diminished. These data suggest that plasma NT levels may be involved in the regulation of GH secretion, as a peripheral signal, probably through modulation of somatostatin release from the median eminence.
Study Information
pubmed
1998
10.1515/jpem.1998.11.5.615