摘要
Obstructive sleep apnea(OSA) is associated with metabolic, cardiovascular and neuropsychological disorders, with substantial morbidity and economic costs. OSA has been estimated to affect 4%-11% of the population, depending on age. Obesity is a significant risk factor for OSA. Non alcoholic fatty liver disease(NAFLD) has emerged as an integral component of the metabolic syndrome, with insulin resistance as the central pathogenic feature. Estimates based on imaging and autopsy studies suggest that about 20%-30% of adults in the United States and other Western countries have NAFLD. Evidence now suggests that NAFLD is independently correlated to insulin resistance regardless of adiposity. Some authors have suggested that OSA may be another contributor to NAFLD development. In complex diseases, several or many different genes interact with environmental factors in determining disease presence or its phenotype. Individual genes only have a small effect on disease risk and can therefore be very difficult to identify. The genetic and hormonal determinants of OSA and NAFLD have received little attention. A wide variety of intermediate phenotypes and genes are involved in OSA and NAFLD which makes this syndrome genetically complex. Various adipokines, the most important of whichare leptin, adiponectin, tumor necrosis factor-alpha, resistin and interleukin-6, have a key role in NAFLD and OSA. Some studies have suggested that oxidative stress may also contribute to the development of NAFLD and OSA. Lifestyle intervention, insulin sensitizer drugs and bariatric surgery aim to improve metabolic syndrome, OSA and NAFLD but need further investigation.
Obstructive sleep apnea(OSA) is associated with metabolic, cardiovascular and neuropsychological disorders, with substantial morbidity and economic costs. OSA has been estimated to affect 4%-11% of the population, depending on age. Obesity is a significant risk factor for OSA. Non alcoholic fatty liver disease(NAFLD) has emerged as an integral component of the metabolic syndrome, with insulin resistance as the central pathogenic feature. Estimates based on imaging and autopsy studies suggest that about 20%-30% of adults in the United States and other Western countries have NAFLD. Evidence now suggests that NAFLD is independently correlated to insulin resistance regardless of adiposity. Some authors have suggested that OSA may be another contributor to NAFLD development. In complex diseases, several or many different genes interact with environmental factors in determining disease presence or its phenotype. Individual genes only have a small effect on disease risk and can therefore be very difficult to identify. The genetic and hormonal determinants of OSA and NAFLD have received little attention. A wide variety of intermediate phenotypes and genes are involved in OSA and NAFLD which makes this syndrome genetically complex. Various adipokines, the most important of whichare leptin, adiponectin, tumor necrosis factor-alpha, resistin and interleukin-6, have a key role in NAFLD and OSA. Some studies have suggested that oxidative stress may also contribute to the development of NAFLD and OSA. Lifestyle intervention, insulin sensitizer drugs and bariatric surgery aim to improve metabolic syndrome, OSA and NAFLD but need further investigation.
