Impact métabolique du SAS : quels mécanismes ? Apports des modèles expérimentaux

Along with other physiopathological conditions, sleep apnea syndrome with chronic intermittent hypoxia and sleep fragmentation generates metabolic disorders such as insulin resistance, dyslipidemia and non-alcoholic fatty liver. Insulin resistance occurs earlier in cases of obesity. Chronic intermittent hypoxia increases hepatic triglyceride content and encourages progression to non-alcoholic fatty liver by increasing activity of the transcription factor HIF-1α. Inflammation and oxidative stress are common mechanisms in various sleep apnea syndrome metabolic complications. Sleep apnea syndrome could be the source of or could exacerbate different components of the metabolic syndrome and therefore exacerbate histologic abnormalities, inducing a switch from fatty liver towards NASH (non-alcoholic steatohepatitis).