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Obstructive sleep apnea and dyslipidemia: implications for atherosclerosis
Luciano F Drager1, Jonathan Jun, Vsevolod Y Polotsky
1Division of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Current Opinion in Endocrinology, Diabetes, and Obesity
|February 4, 2010
Summary
Intermittent hypoxia from obstructive sleep apnea (OSA) can cause hyperlipidemia in mice by activating specific genes. While evidence in humans is inconclusive, OSA treatment may improve lipid profiles.
Area of Science:
- Sleep Medicine
- Metabolic Disorders
- Molecular Biology
Background:
- Obstructive sleep apnea (OSA) is characterized by intermittent hypoxia.
- Dyslipidemia is a common metabolic disorder.
- The relationship between OSA, intermittent hypoxia, and dyslipidemia requires further investigation.
Purpose of the Study:
- To review current evidence on the impact of OSA and intermittent hypoxia on dyslipidemia.
- To provide future research perspectives in this field.
Main Methods:
- Literature review of studies investigating OSA, intermittent hypoxia, and lipid profiles.
- Analysis of molecular mechanisms linking intermittent hypoxia to hyperlipidemia in animal models.
- Evaluation of human studies on OSA and dyslipidemia.
Main Results:
- Intermittent hypoxia induces hyperlipidemia in lean mice, partly via SREBP-1 and stearoyl-CoA desaturase-1 activation.
- Cholesterol biosynthesis genes (SREBP-2, HMG-CoA reductase) are unaffected by intermittent hypoxia in mice.
- Human studies show conflicting results on OSA's independent association with dyslipidemia; some suggest a link, others do not.
- Continuous positive airway pressure treatment for OSA may positively impact lipid profiles.
Conclusions:
- Increasing evidence suggests intermittent hypoxia is independently associated with dyslipidemia.
- The causal role of OSA in dyslipidemia remains to be definitively established.
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