AdipoRon treatment partially reverses chronic sleep restriction-induced alterations in hypothalamic clock-gene expression, oxidative stress, and SIRT1/NRF2/HO-1 signaling in male mice
In male mice subjected to 21 days of chronic sleep restriction (18h/day), AdipoRon (10 μg intranasal daily) partially reversed CSR-associated changes in clock-gene expression (Clock, Bmal1, Per1, Cry1), attenuated oxidative stress, reduced LDL and ALT levels, and increased expression of SIRT1/NRF2/HO-1 pathway proteins. CSR alone increased oxidative stress and reduced SIRT1/NRF2/HO-1 expression, while AdipoRon mitigated these effects.
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AdipoRon treatment partially reverses chronic sleep restriction-induced alterations in hypothalamic clock-gene expression, oxidative stress, and SIRT1/NRF2/HO-1 signaling in male mice The current body of evidence comprises 1 study. EvidenceHub rates the overall confidence at 24/100 (low).
The Claim
AdipoRon treatment partially reverses chronic sleep restriction-induced alterations in hypothalamic clock-gene expression, oxidative stress, and SIRT1/NRF2/HO-1 signaling in male mice
This conclusion is most relevant to: Male mice (strain not specified in abstract).
What the Research Shows
The conclusion draws on 1 linked study. Highlights from the cited literature:
- ▸AdipoRon treatment modulates hypothalamic clock-gene expression, oxidative stress, and SIRT1/NRF2/HO-1-related signaling in male mice subjected to chronic sleep restriction. (Brain research, 2026) —
How It Works
The proposed biological pathway:
- ▸Chronic sleep restriction induces oxidative stress in the hypothalamus
- ▸CSR downregulates SIRT1/NRF2/HO-1 pathway proteins
- ▸AdipoRon activates adiponectin receptors, upregulating SIRT1/NRF2/HO-1 signaling
- ▸This reduces oxidative stress and partially normalizes clock-gene expression, mitigating metabolic disturbances
Who Might Benefit
Evidence fit by population:
- ▸Male mice (strain not specified in abstract)
Recommended Dose
10 μg intranasal daily
Limitations & Caveats
Important context when interpreting this evidence:
- ▸Animal study; results may not directly translate to humans
- ▸Only male mice were used; sex-specific effects not examined
- ▸Mechanistic details of AdipoRon's action on clock genes not fully elucidated
- ▸No behavioral or functional outcomes reported (e.g., sleep quality, cognitive performance)
Frequently Asked Questions
What is AdipoRon?▼
AdipoRon is an orally active synthetic agonist of adiponectin receptors (AdipoR1 and AdipoR2), mimicking the effects of adiponectin, including activation of AMPK and PPAR-α pathways.
How does chronic sleep restriction affect the hypothalamus?▼
Chronic sleep restriction disrupts circadian clock-gene expression, increases oxidative stress, and reduces SIRT1/NRF2/HO-1 signaling, contributing to metabolic disturbances.
What dose of AdipoRon was used in this study?▼
The study used intranasal AdipoRon at a dose of 10 μg per mouse daily for 21 days.
Could AdipoRon be a potential treatment for sleep deprivation effects in humans?▼
This is an animal study; while results are promising, further research is needed to determine safety and efficacy in humans.
References
- 1.Mansouri B, Alipour MR, Mohaddes G, Malaei B, Hamidi N, Hesami-Shabestari R, Hosseinkhani M, Farajdokht F. “AdipoRon treatment modulates hypothalamic clock-gene expression, oxidative stress, and SIRT1/NRF2/HO-1-related signaling in male mice subjected to chronic sleep restriction..” Brain research, 2026. PMID: 42556768 DOI: 10.1016/j.brainres.2026.150484