
Obstructive sleep apnea (OSA) is characterized by upper airway collapse during sleep. Chronic intermittent hypoxia, sleep fragmentation, and inflammatory activation are the main pathophysiological mechanisms of OSA. OSA is highly prevalent in obese patients and may contribute to cardiometabolic risk by exerting detrimental effects on adipose tissue metabolism and potentiating the adipose tissue dysfunction typically found in obesity. This chapter will provide an update on: (a) the epidemiological studies linking obesity and OSA; (b) the studies exploring the effects of intermittent hypoxia and sleep fragmentation on the adipose tissue; (c) the effects of OSA treatment with continuous positive airway pressure (CPAP) on metabolic derangements; and (d) current research on new anti-diabetic drugs that could be useful in the treatment of obese OSA patients.
Cardiovascular outcomes, Sleep Apnea, Obstructive, Continuous Positive Airway Pressure, Insulin resistance, Type 2 diabetes, Dyslipidemia, NAFLD, Humans, Sleep Deprivation, Sympathetic activation, Microbiome, Obesity, Hypoxia
Cardiovascular outcomes, Sleep Apnea, Obstructive, Continuous Positive Airway Pressure, Insulin resistance, Type 2 diabetes, Dyslipidemia, NAFLD, Humans, Sleep Deprivation, Sympathetic activation, Microbiome, Obesity, Hypoxia
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