Abstract:The relationship between obstructive sleep apnea (OSA) and non-alcoholic fatty liver disease (NAFLD) has been an issue of great concern. The primary purpose of this study was to determine the influence of OSA on the levels of liver enzymes including alanine transaminase (ALT) and aspartate transaminase (AST). The secondary purpose was to estimate the effect of OSA on the histological lesions of NAFLD, such as steatosis, lobular inflammation, ballooning degeneration, fibrosis, as well as NAFLD activity score (N… Show more
“…An increasing number of clinical studies point out to a potential link between obstructive sleep apnea (OSA), a respiratory disorder featured by nocturnal intermittent hypoxia (IH) and sleep fragmentation, and NAFLD (15)(16)(17)(18). To highlight, both OSA and NAFLD are especially prevalent among obese individuals and, more interestingly, the severity of nocturnal IH positively correlates with histological features of NASH in OSA patients (19).…”
Nocturnal intermittent hypoxia (IH) featuring obstructive sleep apnea (OSA) dysregulates hepatic lipid metabolism and might contribute to the development of non-alcoholic fatty liver disease (NAFLD) observed in OSA patients. However, further research is required to better understanding the molecular mechanisms underlying IH-induced hepatic lipid accumulation. Therefore, the aim of the present study was to determine the effects of OSA on hepatic CD36 expression and the impact of IH by using a mouse model of OSA. Histological analysis, lipid content and CD36 expression were assessed in livers from subjects who underwent liver biopsy and polygraphic study during sleep, and in livers from mice submitted to chronic IH mimicking OSA. Among those who presented OSA features, NAFLD were significantly more frequent than in control subjects with normal respiratory function (77.8 vs. 36.4%, respectively), and showed more severe liver disease. Interestingly, CD36 expression was significantly overexpressed within the liver of OSA patients with respect to controls, and a significant positive correlation was observed between hepatic levels of CD36 and the values of two well-known respiratory parameters that characterized OSA: apnea/hypopnea index (AHI) and oxygen desaturation index (ODI). Moreover, hepatic lipid accumulation as well as induction of hepatic lipogenic genes, and CD36 mRNA and protein expression were significantly higher in livers from mice exposed to IH conditions for 8 weeks than in their corresponding littermates. This study provides novel evidence that IH featuring OSA could contribute to NAFLD setup partly by upregulating hepatic CD36 expression.
“…An increasing number of clinical studies point out to a potential link between obstructive sleep apnea (OSA), a respiratory disorder featured by nocturnal intermittent hypoxia (IH) and sleep fragmentation, and NAFLD (15)(16)(17)(18). To highlight, both OSA and NAFLD are especially prevalent among obese individuals and, more interestingly, the severity of nocturnal IH positively correlates with histological features of NASH in OSA patients (19).…”
Nocturnal intermittent hypoxia (IH) featuring obstructive sleep apnea (OSA) dysregulates hepatic lipid metabolism and might contribute to the development of non-alcoholic fatty liver disease (NAFLD) observed in OSA patients. However, further research is required to better understanding the molecular mechanisms underlying IH-induced hepatic lipid accumulation. Therefore, the aim of the present study was to determine the effects of OSA on hepatic CD36 expression and the impact of IH by using a mouse model of OSA. Histological analysis, lipid content and CD36 expression were assessed in livers from subjects who underwent liver biopsy and polygraphic study during sleep, and in livers from mice submitted to chronic IH mimicking OSA. Among those who presented OSA features, NAFLD were significantly more frequent than in control subjects with normal respiratory function (77.8 vs. 36.4%, respectively), and showed more severe liver disease. Interestingly, CD36 expression was significantly overexpressed within the liver of OSA patients with respect to controls, and a significant positive correlation was observed between hepatic levels of CD36 and the values of two well-known respiratory parameters that characterized OSA: apnea/hypopnea index (AHI) and oxygen desaturation index (ODI). Moreover, hepatic lipid accumulation as well as induction of hepatic lipogenic genes, and CD36 mRNA and protein expression were significantly higher in livers from mice exposed to IH conditions for 8 weeks than in their corresponding littermates. This study provides novel evidence that IH featuring OSA could contribute to NAFLD setup partly by upregulating hepatic CD36 expression.
“…Notably, a study has demonstrated that OSA patients were three times more likely to have NASH compared with subjects without OSA (41). Moreover, clinical evidence suggests a direct relationship between OSA and NAFLD severity (42,45). Interestingly, low O 2 saturation has been proposed as an important NAFLD risk factor in OSA patients: the lower the O 2 saturation, the higher the NAFLD severity (37,46).…”
Section: Clinical Evidences Linking Osa To Nafldmentioning
Non-alcoholic fatty liver disease (NAFLD) is currently the most common chronic liver disease worldwide and comprises varied grades of intrahepatic lipid accumulation, inflammation, ballooning, and fibrosis; the most severe cases result in cirrhosis and liver failure. There is extensive clinical and experimental evidence indicating that chronic intermittent hypoxia, featuring a respiratory disorder of growing prevalence worldwide termed obstructive sleep apnea, could contribute to the progression of NAFLD from simple steatosis, also termed non-alcoholic fatty liver or hepatosteatosis, to non-alcoholic steatohepatitis; however, the molecular mechanisms by which hypoxia might contribute to hepatosteatosis setup and progression still remain to be fully elucidated. In this review, we have prepared an overview about the link between hypoxia and lipid accumulation within the liver, focusing on the impact of hypoxia on the molecular mechanisms underlying hepatosteatosis onset.
“…In addition, several other neurohormonal mechanisms are involved in the links between OSA and T2D, which are summarised in Fig. 3 (30,39,51,65,96,97,98,99,100,101,102,103,104,105,106,107,108,109,110,111,112,113).…”
Section: Mechanisms: Osa Leading To Dysglycaemia and T2dmentioning
confidence: 99%
“…One plausible mechanism in patients with pre-diabetes or diabetes is autonomic neuropathy, which might impact on UA innervation (6), ventilatory drive and central respiratory responses to hypercapnia (109,110). In addition, T2D is associated with reduced pulmonary volumes and functions compared to healthy individuals which could affect UA stability (111,112,113,114,115,116,117,118,119,120,121) and diffusion capacity for carbon monoxide (112,113,122,123). The impact of T2D on the lungs seems to be related to the severity of hyperglycaemia independently of obesity and smoking (123), which raises the possibility that improvements in glycaemic control might have a favourable impact on OSA.…”
Obstructive sleep apnoea (OSA) is a common disorder that is associated with serious comorbidities with a negative impact on quality of life, life expectancy and health costs. As OSA is related to obesity and is associated with sleep disruption, increased inflammation and oxidative stress, it is not surprising that OSA has an impact on the secretion of multiple hormones and is implicated in the development of many endocrine conditions. On the other hand, many endocrine conditions that can affect obesity and/or upper airways anatomy and stability have been implicated in the development or worsening of OSA. This bidirectional relationship between OSA and the endocrine system has been increasingly recognised in experimental and epidemiological studies and there are an increasing number of studies examining the effects of OSA treatment on endocrine conditions and vice versa. In this review article, we will critically appraise and describe the impact of OSA on the endocrine system including obesity, dysglycaemia, the pituitary, the thyroid, the adrenals, the reproductive system and the bones. In each section, we will assess whether a bidirectional relationship exists, and we will describe the potential underlying mechanisms. We have focused more on recent studies and randomised controlled trials where available and attempted to provide the information within clinical context and relevance.
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