Growth hormone (GH) secretion in the conscious rat: negative feedback of GH on its own release.
Clark. R G RG; Carlsson. L M LM; Robinson. I C IC
Key Findings
- IV GH infusion (20‑60 µg/h) suppresses spontaneous GH pulses in both male and female rats
- The suppression builds up slowly and there’s no immediate rebound when the infusion ends; GH levels gradually normalize
- GH does not block the pituitary’s response to repeated GH‑releasing factor (GRF) injections, suggesting feedback occurs upstream of the pituitary, likely by reducing GRF release
Practical Outcomes
- For biohackers using GH or GH‑releasing peptides like sermorelin, continuous high‑dose GH may blunt your own GH production, potentially lowering overall benefits. Intermittent or low‑dose regimens that avoid constant GH exposure could help maintain natural GH pulses and improve effectiveness.
Summary
In rats, giving growth hormone (GH) continuously through an IV reduces the body’s own natural GH bursts, but it doesn’t stop the pituitary from responding when a GH‑releasing signal is added. The feedback seems to happen higher up in the brain, not directly at the pituitary. When the GH infusion stops, the body slowly returns to normal GH release.
Abstract
The negative-feedback effects of GH on its own secretion were studied in conscious male and female rats bearing indwelling double-bore venous cannulae. Intravenous infusions of human GH (hGH; 20-60 micrograms/h) or somatostatin (SS; 10 micrograms/h) were given while frequent serial microsamples of blood were withdrawn using an automatic blood-sampling system. In both sexes, i.v. infusions of hGH for 6 h inhibited endogenous GH secretory pulses, with a slow onset of the inhibition. There was no rebound GH secretion immediately following the removal of the hGH infusion, but spontaneous GH secretion gradually returned to normal. Infusions of hGH did not inhibit the pituitary GH response to repeated GH-releasing factor (GRF) injections (1 microgram) given i.v. every 40 min to female rats. By contrast, infusions of SS, which also blocked spontaneous GH release, dramatically reduced the GH responses to serial GRF injections. When SS Infusions were stopped, the subsequent GRF-induced GH secretory responses were enhanced. These results show that GH can inhibit its own release when given by i.v. infusion to conscious male and female rats. Since GH responses to GRF are maintained during a GH infusion, the feedback effect of GH is unlikely to be exerted directly on the pituitary or by increasing SS release. Our results are consistent with the idea that GH feedback in the conscious rat involves an inhibition of GRF release.
Study Information
pubmed
1988
10.1677/joe.0.1190201