Obstructive sleep apnea, intermittent hypoxia and non-alcoholic fatty liver disease

With the current epidemic of obesity worldwide, the prevalence of various obesity-related diseases is constantly increasing. Obesity remains the strongest phenotypic risk factor in both obstructive sleep apnea (OSA) and non-alcoholic fatty liver disease (NAFLD). In OSA, intermittent hypoxia-reoxygenation and sleep fragmentation, as a result of recurrent episodes of upper airway obstruction during sleep, may give rise to a plethora of metabolic derangements downstream. Intermittent hypoxia (IH) is postulated to be an important mechanistic trigger for potential systemic impact on organs or tissues in OSA, and has served as a useful experimental model for seeking evidence for downstream effects of OSA. This narrative review focuses on the clinical association between OSA and NAFLD, and the role of IH in the progression of NAFLD in lean and diet-induced obese animal models. Understanding the roles of obesity and IH on NAFLD would advance our limited knowledge on the potential health consequences of OSA, a disease which is afflicting more and more people globally, and also in devising effective therapeutic strategies for this progressively common liver condition.