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DSIP

Emideltide, DSIP nonapeptide, Delta sleep-inducing peptide

Quick Stats
Studies 458
Trials 82
Score 3
1988 pubmed

Evidence for a role of delta sleep-inducing peptide in slow-wave sleep and sleep-related growth hormone release in the rat.

Iyer. K S KS; Marks. G A GA; Kastin. A J AJ; McCann. S M SM

Key Findings

  • Sleep‑deprived rats showed a sharp rise in plasma growth hormone and slow‑wave sleep after the deprivation period.
  • Injecting an antibody that neutralizes DSIP blocked both the increase in deep sleep and the growth hormone surge.
  • Direct injection of DSIP into the brain’s third ventricle previously has been shown to raise growth hormone levels.

Practical Outcomes

  • For biohackers, this study hints that DSIP could be a tool to enhance deep sleep and possibly stimulate growth hormone release after poor sleep, but the evidence is limited to rats. Until human data are available, any self‑experiment should start with very low doses, monitor sleep architecture, and consider safety and regulatory issues.

Summary

In rats, a peptide called delta sleep‑inducing peptide (DSIP) appears to boost deep (slow‑wave) sleep and trigger a spike in growth hormone after a short period of sleep loss. Blocking DSIP stopped these effects, suggesting the peptide naturally helps the body recover sleep and release growth hormone.

Abstract

To examine the role of delta sleep-inducing peptide (DSIP) in sleep-related growth hormone (GH) release, male rats were deprived of sleep for 4 hr by placing them on a slowly rotating wheel. Sleep deprivation by this method caused a significant increase in GH release, as indicated by the increase in plasma GH concentrations (P less than 0.01), and also in the amount of slow-wave sleep (SWS) (P less than 0.001) above initial values after removal of the animals from the rotating wheel. These increases were blocked by microinjection into the third cerebral ventricle of highly specific antiserum to DSIP. In control rats receiving an equal volume of normal rabbit serum, the significant increase in plasma GH as well as SWS remained after removal of the rats from the wheel. The increased release of endogenous DSIP in the sleep-deprived animals may have caused an increase in SWS as well as plasma GH. Since DSIP increases plasma GH after its injection into the third cerebral ventricle and since passive immunization against DSIP blocks the increase in SWS and GH release that follows the 4 hr of sleep deprivation, the results suggest that DSIP can be a physiological stimulus for sleep-related GH release as well as for the induction of SWS.

Study Information

Provider

pubmed

Year

1988

DOI

10.1073/pnas.85.10.3653