ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Targeted Delivery of CNS-Specific Hesperidin as a Leptin Sensitizer for Treating Obesity-Associated Sleep-Disordered Breathing.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Restoring leptin sensitivity in metabolic and extra-metabolic leptin resistance: Pharmacologic strategies, systemic implications, and future directions.EXCLI journal · 2026Review
- Targeted Delivery of CNS-Specific Hesperidin as a Leptin Sensitizer for Treating Obesity-Associated Sleep-Disordered Breathing.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Bidirectional crosstalk between sleep disorders and gynecological cancers: unraveling molecular synergies and precision therapeutics.Frontiers in medicine · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
Obesity-associated obstructive sleep apnea (OSA) highlights the need for effective therapies. Hypothalamic endoplasmic reticulum (ER) stress contributes to leptin resistance in obesity. Although hesperidin (HE) modulates ER stress and oxidative pathways, its low bioavailability limits clinical use, its role in OSA is unknown. Self-assembled HE nanoparticles (HE NPs) are developed to address this. HE NPs are synthesized via solvent emulsification-evaporation and tested in diet-induced obese (DIO), lean, and ob/ob mice. In DIO mice, HE NPs reduce food intake, body weight, and plasma leptin while mitigating hypothalamic ER stress and boosting STAT3 phosphorylation, without toxicity, and they outperform HE and PLGA NPs. In ob/ob mice, HE NPs lower PERK phosphorylation and, with leptin, further suppress weight gain and food intake while enhancing STAT3 signaling. Combining HE NPs with leptin in DIO mice amplifies weight loss versus HE NPs alone. HE NPs also improve sleep-disordered breathing, lowering the apnea index during non-rapid eye movement sleep (17.1±3.5 to 9.3±3.0 events h
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.