Nonalcoholic fatty liver disease and obstructive sleep apnea.
Obstructive sleep apnea (OSA) and more importantly its hallmark, chronic intermittent hypoxia (CIH), are established factors in the pathogenesis and exacerbation of nonalcoholic fatty liver disease (NAFLD). This has been clearly demonstrated in rodent models exposed to intermittent hypoxia, and strong evidence now also exists in both paediatric and adult human populations. OSA and CIH induce insulin-resistance and dyslipidemia which are involved in NAFLD physiopathogenesis. CIH increases the expression of the hypoxia inducible transcription factor HIF1α and that of downstream genes involved in lipogenesis, thereby increasing β-oxidation and consequently exacerbating liver oxidative stress. OSA also disrupts the gut liver axis, increasing intestinal permeability and with a possible role of gut microbiota in the link between OSA and NAFLD. OSA patients should be screened for NAFLD and vice versa those with NAFLD for OSA. To date there is no evidence that treating OSA with continuous positive airway pressure (CPAP) will improve NAFLD but it might at least stabilize and slow its progression. Nevertheless, these multimorbid patients should be efficiently treated for all their metabolic co-morbidities and be encouraged to follow weight stabilization or weight loss programs and physical activity life style interventions.
Institute of Cardiometabolism and Nutrition, ICAN, Assistance Pitié-Salpêtrière Hospital, Paris, France; Sorbonne Universités, Université Pierre et Marie Curie-Paris 6, UMR_S U1166, Nutriomics, 75013 Paris, France; INSERM, UMR_S U1166, Nutriomics, 75013 Paris, France. Electronic address: judith.aron-wisnewsky@psl.aphp.fr.
Judith
J
Aron-Wisnewsky
Institute of Cardiometabolism and Nutrition, ICAN, Assistance Pitié-Salpêtrière Hospital, Paris, France; Sorbonne Universités, Université Pierre et Marie Curie-Paris 6, UMR_S U1166, Nutriomics, 75013 Paris, France; INSERM, UMR_S U1166, Nutriomics, 75013 Paris, France.
Karine
K
Clement
Institut National de la Santé et de la Recherche Médicale (INSERM), U 1042, HP2 Laboratory (Hypoxia: Pathophysiology), Grenoble Alpes Univ., Grenoble, F-38000, France;; Grenoble Alpes University Hospital, Pole Thorax et Vaisseaux, F-38000, France. Electronic address: jpepin@chu-grenoble.fr.
Jean-Louis
JL
Pépin
D006801:Humans; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000378:metabolism; D007333:Insulin Resistance / Q000502:physiology; D050155:Lipogenesis / Q000502:physiology; D008099:Liver / Q000378:metabolism*; D065626:Non-alcoholic Fatty Liver Disease / Q000209:etiology* / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology*; D020181:Sleep Apnea, Obstructive / Q000150:complications* / Q000378:metabolism
C497442:HIF1A protein, human; D051795:Hypoxia-Inducible Factor 1, alpha Subunit
Chronic intermittent hypoxia; Nonalcoholic fatty liver disease; Obstructive sleep apnea