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DSIP

Emideltide, DSIP nonapeptide, Delta sleep-inducing peptide

Quick Stats
Studies 458
Trials 82
Score 2
2012 pubmed 6 citations

Effect of delta sleep-inducing peptide on oxidative modification of proteins in rat tissues and blood during physiological aging.

Bondarenko. T I TI; Sorokina. I A IA; Mayboroda. E A EA; Durkanaeva. O A OA; Kutilin. D S DS; Mikhaleva. I I II

Key Findings

  • DSIP (100 µg/kg) administered subcutaneously in 5‑day monthly courses reduced protein carbonyl and increased sulfhydryl groups, indicating less oxidation in spleen, heart, testicles, liver, and muscle.
  • The protective effect was tissue‑specific, with the spleen showing the greatest benefit.
  • DSIP lowered blood glucose‑related damage by preventing non‑enzymatic glycation of hemoglobin.

Practical Outcomes

  • The results suggest DSIP might have antioxidant and mild blood‑sugar‑lowering properties, but the evidence is limited to rats and uses injectable dosing that isn’t established for humans. Biohackers should view this as early‑stage data; more research is needed before considering DSIP for personal longevity protocols.

Summary

A study in aging rats found that giving delta sleep‑inducing peptide (DSIP) under the skin once a month for five days helped protect proteins in several organs from oxidative damage and lowered blood sugar‑related protein changes. The effect varied by tissue, and the peptide also reduced the formation of glycated hemoglobin, a marker of high blood sugar.

Abstract

Accumulation of oxidized proteins (evaluated by the levels of carbonyl and SH groups) in tissues of 2-24-month-old rats (spleen>myocardium>testicles>liver>skeletal muscles) has been demonstrated. Exogenous delta sleep-inducing peptide injected subcutaneously to rats of different age in a dose of 100 μg/kg by monthly 5-day courses protected proteins of the studied tissues from oxidation; its effect was tissue-specific. Delta sleep-inducing peptide exhibited a hypoglycemic effect: it prevented nonenzymatic glycosylation of hemoglobin and reduced the level of defective protein molecules during aging.

Study Information

Provider

pubmed

Year

2012

Date

2012-07-01T00:00:00.000Z

DOI

10.1007/s10517-012-1719-3

Citations

6

References

12