Association Between Metabolic-Associated Fatty Liver Disease and Obstructive Sleep Apnea: A Cross-Sectional Study

Abstract

Aim Emerging evidence has revealed that obstructive sleep apnea (OSA) is an independent risk factor for the development of a variety of adverse metabolic disease states. In this study, we evaluated the association between OSA severity and metabolic dysfunction-associated fatty liver disease (MAFLD) among Asian populations. Materials and Methods This was a cross-sectional, single-center study. The study cohort consisted of patients undergoing polysomnography and abdominal ultrasonography. Logistic regression analysis was used to evaluate the independent risk factors of MAFLD in patients with OSA. Results A total of 1065 patients (277 non-MAFLD and 788 MAFLD) were included in the study. The prevalence of MAFLD in non-OSA, mild-moderate OSA, and severe OSA patients was 58.16%, 72.41%, and 78.0%, respectively ( p < 0.001). We identified significant differences in body mass index (BMI), apnea-hypopnea index (AHI), oxygen desaturation index (ODI), and lowest O 2 saturation (LaSO 2 ) between non-MAFLD and MAFLD patients (all p < 0.001). After adjusting for confounding variables, we used multivariate regression analysis to show that BMI, ODI, and triglyceride (TG) levels independently predicted the occurrence of MAFLD (odds ratio [OR] = 1.234, p < 0.001; OR = 1.022, p = 0.013; OR = 1.384, p = 0.001, respectively). Moreover, stratified analysis according to BMI indicated that TG levels were the predominant risk factor for MAFLD in a group of patients with a BMI < 23 kg/m 2 , while BMI, ODI, TG levels, and total cholesterol (TC) were the major risk factors for MAFLD in a group of patients with a BMI ≥ 23 kg/m 2 (all p < 0.05). Conclusion OSA-associated chronic intermittent hypoxia was independently associated with the risk of MAFLD, especially in OSA patients with a BMI ≥ 23 kg/m 2 , suggesting that oxidative stress might play an important role in the pathogenesis of MAFLD in patients with OSA.

Loss of testosterone induces postprandial insulin resistance and increases the expression of the hepatic antioxidant flavin‐containing monooxygenases in mice exposed to intermittent hypoxia

“…This coincided with lower body and fat masses and a reduced fat/lean mass ratio in ORX‐IH versus the Sham‐IH, Sham‐Nx, and ORX‐Nx mice, and with the establishment of a hepatic pro‐oxidant profile of enzyme activity. The bulk of evidence indicate that disturbed fat metabolism, postprandial insulin resistance, and hepatic oxidative stress are key elements that contribute to the development of liver diseases, 3,24 and type II diabetes 13,25,26 . On the other hand, the liver plays an important role in whole‐body glucose homeostasis, particularly through the timely regulated balance of sympathetic and vagal nerves activity during the postprandial period 27 .…”

“…22 Contrastingly, during the physiological post-prandial period induced by prolonged fasting (12 h) immediately followed by refeeding (2 h), there were relative hypoglycemia and hyperinsulinemia, and the HOMA-IR index was higher in ORX-IH mice compared to the other groups. stress are key elements that contribute to the development of liver diseases, 3,24 and type II diabetes. 13,25,26 On the other hand, the liver plays an important role in wholebody glucose homeostasis, particularly through the timely regulated balance of sympathetic and vagal nerves activity during the postprandial period.…”

“…2 Oxidoreductase activity, acting on paired donors, with incorporation or reduction of molecular oxygen, reduced flavin or flavoprotein as one donor, and incorporation of one atom of oxygen. 3 Transferase activity, transferring phosphorus-containing groups. increases mRNA and protein hepatic FMO3 expression, and FMO3 overexpression mimics the robust beneficial antioxidant effects of caloric restriction on the liver, including a decreased MDA level and increased SOD activity.…”

“…Sleep apnea (SA) is a highly prevalent respiratory disorder associated with metabolic dysfunctions 1,2 and non‐alcoholic fatty liver disease 3 . The association between SA and metabolic diseases is clearly attributable to the episodes of nocturnal intermittent hypoxia (IH) that increase the activity of the sympathetic nervous system and induce insulin resistance 4,5 as well as oxidative stress in the liver 6,7 and adipose tissue 8 .…”

“…Sleep apnea (SA) is a highly prevalent respiratory disorder associated with metabolic dysfunctions 1,2 and nonalcoholic fatty liver disease. 3 The association between SA and metabolic diseases is clearly attributable to the episodes of nocturnal intermittent hypoxia (IH) that increase the activity of the sympathetic nervous system and induce insulin resistance 4,5 as well as oxidative stress in the liver 6,7 and adipose tissue. 8 In the liver, oxidative stress induced by IH occurs despite an increased expression of superoxide dismutase (SOD-one of the main antioxidant enzymes) and specific enrichment of genes regulated by the Nuclear Respiratory Factor 1 and 2 (NRF1-NRF2, two of the main transcription factors that orchestrate cellular and mitochondrial responses to oxidative stress) as assessed by transcriptomic analysis.…”