DSIP
Delta Sleep–Inducing Peptide (DSIP) is a naturally occurring nonapeptide first identified in 1977 during investigations of mammalian sleep regulation. Although originally isolated for its sleep-related activity, subsequent research characterizes DSIP as a multifaceted neuromodulatory peptide involved in neuroendocrine signaling, stress adaptation, and cellular protection. DSIP has been detected in the hypothalamus, pituitary, and peripheral tissues, where it appears to act as a mediator between the central nervous, endocrine, and immune systems.
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The information provided is for educational and informational purposes only and should not be interpreted as medical advice. All products described herein are intended strictly for laboratory and research use. They are not approved for human or veterinary administration, and should only be handled by qualified professionals in controlled research environments. Any clinical research must be conducted under the supervision and approval of an Institutional Review Board (IRB), and all preclinical studies must adhere to Institutional Animal Care and Use Committee (IACUC) guidelines in accordance with the Animal Welfare Act (AWA). Users are encouraged to conduct their own due diligence, referencing trusted scientific sources and verifying all information independently before making any purchasing or experimental decisions.
⚠️ Notice: All products are sold for laboratory and research purposes only. They are not intended for diagnostic, therapeutic, or personal use under any circumstances.
DSIP
Overview
Delta Sleep–Inducing Peptide (DSIP) is a naturally occurring nonapeptide first identified in 1977 during investigations of mammalian sleep regulation. Although originally isolated for its sleep-related activity, subsequent research characterizes DSIP as a multifaceted neuromodulatory peptide involved in neuroendocrine signaling, stress adaptation, and cellular protection. DSIP has been detected in the hypothalamus, pituitary, and peripheral tissues, where it appears to act as a mediator between the central nervous, endocrine, and immune systems. All observations have been reported in animal or in-vitro experimental settings.
Mechanistic Insights
1. Neuroendocrine Regulation
- DSIP has been observed to influence hypothalamic and pituitary signaling, affecting secretion of GH, LH, and ACTH in preclinical studies via GABAergic and serotonergic pathways that maintain neuroendocrine stability under laboratory stress conditions.
2. Stress-Response Modulation
- In animal models, DSIP has been reported to attenuate hyperactivation of the HPA axis, reducing corticotropin and cortisol levels during controlled stress exposure, suggesting a stress-adaptive role within physiological regulatory systems.
3. Neuroprotective and Antioxidant Mechanisms
- Laboratory data suggest DSIP may reduce oxidative damage and lipid peroxidation in neuronal tissues, supporting mitochondrial membrane stability and reducing apoptosis under in-vitro oxidative-stress conditions.
4. Sleep Regulation Mechanisms
- Experimental models have shown DSIP can modify EEG slow-wave (delta) activity and restore typical REM–non-REM cycling patterns in animals, likely related to GABAergic modulation and circadian rhythmic control via the hypothalamic-pineal axis.
Key Research Observations
1. Sleep Architecture and Recovery
- Increased delta-wave EEG amplitude and prolonged slow-wave phases observed in rodents.
- Decreased latency to sleep onset in controlled animal studies.
- Associated with heightened nocturnal GH secretion under experimental conditions.
- Stabilization of circadian rhythms following stress exposure in laboratory settings.
2. Stress Adaptation and Cortisol Dynamics
- Decreased ACTH and corticosterone release under induced stress paradigms.
- Normalization of autonomic variability indices in rodent stress-response assays.
- Exhibited adaptogenic-like modulation in prolonged fatigue models.
3. Hormonal and Metabolic Regulation
- Induction of pulsatile GH and LH secretion in isolated pituitary assays.
- Down-regulation of stress-associated ACTH output in animal endocrine studies.
- Maintenance of rhythmic hormone expression consistent with circadian stability.
4. Neuroprotection and Cognitive Processes
- Attenuation of neuronal oxidative injury in ischemia and hypoxia models.
- Facilitation of learning performance in rodent mazes under fatigue conditions.
- Regulation of neurotransmitter turnover contributing to synaptic plasticity.
5. Nociception and Inflammatory Modulation
- Modulation of pain thresholds via interaction with opioid-receptor pathways.
- Synergistic interaction with endorphin peptides documented in analgesia studies.
- Reduced neurogenic inflammation observed in controlled preclinical assays.
6. Antioxidant and Cellular Homeostasis
- Up-regulation of SOD and catalase activity in in-vitro oxidative models.
- Decrease in lipid peroxidation and DNA oxidation metrics.
- Stabilization of mitochondrial energetics and reduction of apoptotic signaling.
7. Immune and Mood-Related Research
- Balanced cytokine expression profiles in animal immune-stress assays.
- Improved metabolic regulation under sleep-restriction paradigms.
- Adjustment of serotonin–dopamine tone linked to emotional stability.
Research References
- Monnier M. et al. (1977). Proc Natl Acad Sci USA.
- Graf M. V. et al. (1984). Neuropeptides.
- Sudakov K. V. et al. (1986). Exp Brain Res.
- Antonijevic I. et al. (1990). J Neural Transm.
- Matsumoto K. et al. (1988). Peptides.
- Przewłocka B. et al. (1983). Pol J Pharmacol Pharm.
- Sudakov K. V. et al. (1998). Neurosci Behav Physiol.
- Dubrovina N. I., Alekseeva E. V. (2007). Neurosci Lett.
- Bubenik G. A. et al. (2000). Int J Neurosci.
- Basile A. S. et al. (1981). Brain Res.
Product Specifications
C₃₅H₄₈N₁₀O₈
848.84 g/mol
62568-57-4
Delta Sleep-Inducing Peptide
Lyophilized powder
Keep refrigerated upon reconstitution
Soluble in sterile water and 0.9% NaCl solution
Research-use only. All information summarizes preclinical and in-vitro studies and is not intended for diagnostic, therapeutic, or personal use.
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