Abstract
Obstructive sleep apnea (OSA) syndrome has emerged as a major public health problem because of its high prevalence amongst middle-aged, obese men as well as in lean individuals and women. It has been suggested that obesity’s role in the genesis of sleep apnea is rather through its metabolic activity than a purely anatomic / mechanical impact. Recent studies demonstrate that circulating levels of adipocytes, adipose tissue-derived secretory proteins, are altered in patients with OSA syndrome. For in- stance, leptin level is increased, whereas that of adiponectin decreased in OSA, and these changes can be reversed by treatment of apnea/hypopnea episodes. Adipokine profile seems to change towards a pro inflammatory pattern that may also contribute to OSA-related cardio metabolic diseases. The mechanisms of adipose dysfunction in OSA includes hypoxia, oxidative stress and increased sympathetic nervous activity, including alterations in the circulating levels of the neurotrophins nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF). In effect, reversing hypoxia and attenuating oxidative stress and inflammation through adipokine and NGF/BDNF- targeted pharmacology may provide novel therapeutic opportunities in patients with OSA syndrome.
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