Delta sleep-inducing peptide (DSIP) stimulates growth hormone (GH) release in the rat by hypothalamic and pituitary actions.
Iyer. K S KS; McCann. S M SM
Key Findings
- Intraventricular injection of DSIP raises plasma GH in rats, with effects starting at 0.1āÆĀµg and peaking around 10āÆĀµg.
- The GH increase is blocked by the dopamine receptor antagonist pimozide, suggesting a dopaminergic mechanism.
- Cultured pituitary cells also release more GH when exposed to DSIP, with the strongest response at 10ā»Ā¹Ā²ā10ā»Ā¹ā°āÆM, but higher concentrations lose effectiveness.
Practical Outcomes
- DSIP shows potential to stimulate growth hormone, but the only effective delivery in this study was direct brain injection, which isnāt feasible for humans. Thereās no evidence yet that oral or injectable DSIP works the same way, so biohackers should treat this as a preliminary finding rather than a readyātoāuse protocol.
Summary
In rats, the peptide delta sleepāinducing peptide (DSIP) raises growth hormone levels when injected into the brain or added to pituitary cells, and this effect seems to involve dopamine signaling. The hormone boost is doseādependent but tops out at about a 50% increase over normal levels. The study was done in ovariectomized rats and used direct brain injections, so it doesnāt tell us how DSIP works when taken as a supplement in humans.
Abstract
To evaluate possible effects of delta sleep-inducing peptide on GH release, the peptide was micro-injected into conscious animals with third ventricular cannulae and blood samples were drawn from indwelling external jugular vein cannulae. Ovariectomized animals were used in order to eliminate gonadal steroid feedback. In the initial experiment, intraventricular injection of 5 micrograms of the peptide induced an elevation of GH which became significant by 30 min and persisted for the 120 min duration of the experiment after the injection. Diluent-injected animals showed a slight initial drop in GH and then no increase. The increase in plasma GH induced by the peptide was dose-related with a minimal effective dose of 0.1 microgram and a linear log-dose increase to a dose of 10 micrograms. This effect is presumably mediated hypothalamically via a dopaminergic mechanism since it could be blocked by pre-treatment of the animals with pimozide, a dopamine receptor blocker. Dispersed overnight, cultured pituitary cells from ovariectomized rats exhibited a dose-related increase in GH release in static incubations with DSIP. A response occurred with the lowest dose tested (10(-12) M) which increased to a maximum at 10(-10) M DSIP. The responses then declined at higher doses such that they were no longer significant at doses of 10(-7) and 10(-5) M. The increase even at the most effective dose was approximately 50% above the basal values. The results are consistent with the hypothesis that DSIP may be involved in GH release via a dopaminergic mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)
Study Information
pubmed
1987
10.1016/0196-9781(87)90163-x