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Decreased plasma levels of orexin-A in sleep apnea

Xavier Busquets1, Ferran Barbé, Antonia Barceló

  • 1Unidad de Investigación, Hospital Universitari Son Dureta, Palma de Mallorca, Spain.

Respiration; International Review of Thoracic Diseases
|January 4, 2005
PubMed
Abstract

Insights

Orexin-A levels are significantly lower in patients with obstructive sleep apnea syndrome (OSAS), regardless of obesity or sleepiness. Continuous positive airway pressure (CPAP) treatment did not normalize these low orexin-A levels in OSAS patients.

Area of Science:

  • Neuroscience
  • Sleep Medicine
  • Endocrinology

Background:

  • Orexin-A (hypocretin) is a neuropeptide crucial for regulating appetite and sleep-wake cycles.
  • Obstructive sleep apnea syndrome (OSAS) is associated with obesity and excessive daytime sleepiness.
  • The role of orexin-A in OSAS pathogenesis and the impact of continuous positive airway pressure (CPAP) treatment remain unclear.

Purpose of the Study:

  • To investigate plasma orexin-A levels in patients with OSAS.
  • To determine the effect of CPAP treatment on orexin-A levels in OSAS patients.

Main Methods:

  • A comparative study involving 13 healthy controls, 27 untreated OSAS patients, and 14 OSAS patients treated with CPAP for at least one year.
  • Plasma orexin-A levels were measured using established assays.
  • Severity of OSAS was quantified by the apnea-hypopnea index (AHI).

Main Results:

  • Plasma orexin-A levels were significantly lower in both untreated (9.4 ± 1.9 pg/mL) and CPAP-treated (4.2 ± 1.5 pg/mL) OSAS patients compared to healthy controls (20.6 ± 4.5 pg/mL).
  • In untreated OSAS patients, orexin-A levels did not correlate significantly with daytime somnolence (Epworth scale) or body mass index.
  • CPAP treatment did not restore orexin-A levels to those observed in healthy individuals.

Conclusions:

  • Patients with OSAS exhibit significantly reduced plasma orexin-A levels.
  • Low orexin-A levels in OSAS are independent of somnolence severity and obesity.
  • These findings suggest a potential role for diminished orexin-A in the pathophysiology of OSAS.

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