ABSTRACT
Sleep-disordered breathing, a widespread condition, leads to obstructive sleep apnea syndrome, which is associated with severe health consequences including metabolic disorders, cardiovascular diseases, and diabetes. OSA has been recognized more frequently in obese individuals as the intermittent airway obstruction during sleep with frequent arousals, thus establishing links between obesity, sleep-induced airway obstruction, sleep fragmentation, and daytime sleepiness. Adipose tissue secretes pro-infl ammatory cytokines and hormonelike molecules called adipokines such as the interleukins (IL), tumor necrosis factor α (TNF-α), leptin, and adiponectin. Th ese adipose-derived cytokines and adipokines exert a profound impact on the neural pathways of respiratory control. Leptin has been shown to act as a respiratory stimulant and is associated with obesity hypoventilation syndrome. Obesity and OSA have been shown to be associated with elevated circulating levels of leptin and impaired leptin signaling appears to contribute to respiratory depression. Leptin is also implicated in nocturnal hypoventilation during sleep. Pro-infl ammatory cytokines such as TNF-α, IL-1β, and IL-6 secreted by visceral adipose tissue seem to be involved in physiological sleep regulation. Adiponectin, another important anti-atherogenic adipokine, is secreted exclusively and abundantly by adipose tissue. Although signifi cant reduction in circulating adiponectin levels in obese individuals has
*Corresponding author
been documented, the eff ect of sleep apnea on circulating adiponectin levels in OSA patients, particularly on the biologically active high molecular weight form, is unclear. Th e association between adipose-derived adipokines and sleep disorders such as OSA is emerging and more studies in this area are needed.
