Delta-sleep-inducing peptide (DSIP) inhibited CRF-induced ACTH secretion from rat anterior pituitary gland in vitro.
Okajima. T T; Hertting. G G
Key Findings
- DSIP at 10â»âžâŻM most strongly blocked CRFâtriggered ACTH release from rat pituitary tissue.
- DSIP lowered the CRFâinduced rise in cAMP, a key second messenger in hormone secretion.
- DSIP had no effect on baseline ACTH or cAMP levels and did not alter prostaglandin E2 release.
Practical Outcomes
- The data suggest DSIP could blunt stressâinduced ACTH (and downstream cortisol) spikes, hinting at a possible stressâmodulating use. However, the study is limited to rat cells in vitro, so thereâs no direct guidance on human dosing or safety. Biohackers should treat this as earlyâstage evidence and await human studies before adding DSIP for stress control.
Summary
In a lab test using rat pituitary cells, the peptide DSIP reduced the release of the stress hormone ACTH when the cells were stimulated, likely by blocking a signaling molecule called cAMP. It didnât change hormone levels on its own and didnât affect other pathways like prostaglandin release.
Abstract
Delta-sleep-inducing peptide (DSIP, 10(-9) - 10(-7) M) significantly inhibited the CRF-induced ACTH release from rat anterior pituitary quarters in vitro. 10(-8) M DSIP showed the most prominent inhibition. DSIP (10(-8) M) also inhibited the CRF-activated cAMP levels in anterior pituitary tissue. DSIP did not influence basal ACTH or cAMP levels. Prostaglandin E2 (PGE2)-release from anterior pituitary quarters was not changed by DSIP. From these results, we conclude that DSIP inhibits CRF-induced ACTH release at the pituitary level through the inhibition of the cAMP system in corticotrophs. The involvement of PGE2 in this phenomenon is unlikely.
Study Information
pubmed
1986
1986-07-01T00:00:00.000Z
10.1055/s-2007-1012357
21
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