Obstructive Sleep Apnea Hypopnea Syndrome (OSAHS) is a common disease, mainly seen in middle-aged obese men, and the prevalence of OSAHS in adult males in the general population is about 2-4% in adult males who fulfill the current diagnostic criteria of clinical and polysomnography (PSG); while the prevalence of OSAHS in adult females is about 1-2% if PSG alone is used as the diagnostic criterion (i.e. Apnea-Hypopnea Index). In the general population, the prevalence is 2-4% in adult males and 1-2% in adult females who meet the current clinical and polysomnographic (PSG) diagnostic criteria, while the prevalence is 17-24% in males and 5-9% in females when PSG alone is used as a diagnostic criterion (i.e., Apnea-Hypopnea Index (AHI) > 5/hour of sleep), but most of these patients do not have daytime sleepiness and/or cardiovascular problems. Problems. In addition to daytime sleepiness, OSAHS is often associated with insulin resistance and cardiovascular risk factors such as hypertension, obesity, and diabetes mellitus. Even in mild OSAHS, the incidence of pulmonary hypertension, circulatory hypertension, and cardiac arrhythmias is significantly higher, and the morbidity and mortality from cardiovascular and cerebral vascular diseases are significantly higher. However, it is not clear whether these conditions are a consequence of the long-term effects of other factors typical of patients with OSAHS, such as hypertension, centripetal obesity, insulin resistance, and hyperlipidemia, or whether they are a direct result of OSAHS itself, which leads to reduced patient survival. Obstructive sleep apnea events can lead to many acute pathophysiologic changes such as intermittent hypoxia, severe sleep fragmentation, acute blood pressure elevation, sympathetic nervous system activation, changes in intrathoracic pressure, and decreased cardiac output, which can eventually lead to hypertension and cardiovascular disease in the long term, and the independent relationship between sleep apnea and glucose metabolism abnormality may represent another cardiovascular disease causing The metabolic syndrome (The metabolic syndrome) The metabolic syndrome (MS) was proposed as a name in 1981 and agreed upon by a WHO expert panel in 1998 to describe a collection of interrelated risk factors for metabolic disorders such as abdominal obesity, elevated triglycerides, lowered high-density lipoprotein (HDL), hypertension, and hyperglycemia. According to the National Cholesterol Program (NCEP) Adult Treatment Panel III guidelines (ATP III), metabolic syndrome is diagnosed if three of the following five factors are present: increased waist circumference, elevated blood pressure, elevated fasting blood glucose levels, elevated triglyceride levels, and decreased HDL levels. Other key features of metabolic syndrome include microproteinuria, hypercoagulability, systemic inflammation, endothelial dysfunction, cardiorespiratory hypoplasia, and increased sympathetic nerve activity. All of these factors contribute directly to the development of atherosclerotic cardiovascular disease (ASCVD), and patients with three or more of these components are at particularly high risk of developing ASCVD, as are patients with metabolic syndrome who are at increased risk of developing type II diabetes. Patients with OSAHS also have all of these key components of the metabolic syndrome, so it has been suggested that the metabolic syndrome (syndrome X) should include OSAHS (i.e., syndrome Y). Studies have confirmed that the prevalence of metabolic syndrome in OSAHS is upwards of 40%. A recent study also confirmed that OSAHS and metabolic syndrome have the same age distribution, and that the incidence of both increases with age, peaks at 50-70 years of age, and then gradually decreases, and that menopause in women is also a risk factor for their development. Many of the clinical manifestations of metabolic syndrome are characterized by increased insulin resistance, so this article is intended to focus on the relationship between OSAHS and glucose metabolism. OSAHS and insulin resistance The incidence of insulin resistance and diabetes mellitus is significantly higher in patients with OSAHS than in healthy individuals, and many studies in recent years have confirmed the independent correlation between sleep apnea and glucose metabolism abnormalities.Ip et al [9] confirmed the independent correlation between AHI and the lowest oxygen level during sleep and insulin resistance in a study of 270 patients with OSAHS, and to Cardiovascular obesity (i.e., waist-to-hip ratio, WHR) was also associated with the severity of sleep apnea, and hypertension was significantly associated with insulin resistance; Punjabi and colleagues studied 150 healthy men and noted that the degree of nocturnal hypoxia with AHI was independently associated with impaired glucose tolerance and insulin resistance, while there was no correlation with cardiovascular obesity (WHR). A multicenter, large-sample study confirmed that AHI and mean oxygen levels during sleep were associated with elevated fasting glucose levels and impaired glucose tolerance, and that the severity of sleep apnea was also associated with the degree of insulin resistance, independent of confounding factors such as BMI and waist circumference. A large study confirmed the correlation between AHI and fasting insulin (but not fasting glucose) levels, with apnea patients having higher mean fasting glucose and plasma insulin levels than obese controls, and Ip and colleagues [9] found insulin resistance to be present even in non-obese patients with OSAHS, while Punjabi and colleagues demonstrated that insulin resistance can be present even in mild OSAHS. Ip et al [9] found that the prevalence of insulin resistance increased with increasing age and obesity, but further analysis showed that obesity was a major determinant of insulin resistance, and that the severity of apnea (AHI and minimum oxygen saturation) was also an independent factor in insulin insensitivity. Increased insulin resistance appears to play a key role not only in the metabolic mechanism of action in OSAHS, but also in the metabolic syndrome in general. Hyperinsulinemia increases blood pressure, and it is feared that the main pathophysiologic mechanism of the insulin resistance syndrome is a correlative dissociation between the intermediary metabolic effects of insulin and its growth-promoting effects [especially on the vascular epithelium].Increased insulin resistance in patients with OSAHS has also been repeatedly reported. However, insulin resistance is not uncommon in the general population, but is also associated with obesity, physical inactivity, or the use of various medications, which are also common in OSAHS, and it is these confounding factors that have led to conflicting conclusions in many studies. Intermediate Mechanisms of Abnormal Glycemic Metabolism in Sleep Apnea Basic studies have shown that multiple mechanisms may be involved in the effects of sleep apnea on glucose metabolism: intermittent hypoxia and sleep fragmentation can alter the sympathetic nervous system, the hypothalamic-pituitary-adrenal axis [HPA axis] and the growth hormone axis, increased levels of circulating inflammatory cytokines, and the induction of certain prolipotropic factors and consequent effects on glucose metabolism. Alterations in autonomic nervous system and neuroendocrine function: Possible intermediate pathways by which sleep apnea affects glucose metabolism include the autonomic nervous system and the HPA axis. Many studies have demonstrated increased sympathetic activity in patients with OSAHS. Each obstructive apnea is accompanied by a transient sympathetic activation that recovers after termination of the apneic event. Hypoxemia is an important stimulus affecting autonomic activation, and the lower the blood oxygen level, the more pronounced the increase in sympathetic activation. However, other factors, including hypercapnia and repeated microarousals from sleep, can also lead to increased autonomic output. Increased sympathetic hyperactivity can affect glucose homeostasis by increasing glycogen degradation and glucose production. In addition, sleep apnea may predispose patients to metabolic abnormalities through its effects on the HPA axis. Experimental partial or complete sleep deprivation has demonstrated that plasma corticosterone levels are elevated by 37% and 45%, respectively, and that increased nocturnal corticosterone levels have a significant effect on serum glucose and insulin levels as well as on the rate of insulin secretion. Although sleep deprivation is not the same as fragmented sleep due to OSAHS, the increased sympathetic activation in sleep apnea also increases corticotropin-releasing hormone and corticosterone production. In addition to the negative effects of sleep apnea on the sympathetic nervous system and the HPA axis, multiple studies have confirmed that sleep apnea has a negative effect on growth-promoting hormone function. Sleep apnea can lead to decreased levels of insulin-like growth factor I (IGF-I) produced by the liver and may represent another factor linking sleep apnea to abnormal glucose metabolism. Prospective studies have confirmed that low circulating IGF-I levels are a risk factor for impending reduced glucose tolerance or type II diabetes. Still, the existing view of the independent influence of increased sympathetic activation, HPA axis abnormalities, and growth-promoting hormone function on the development of glucose metabolism abnormalities in sleep apnea is limited. Inflammatory cytokines: Sleep apnea-associated hypoxia may also affect glucose metabolism by promoting the release of inflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). Studies have demonstrated that plasma levels of IL-6 and TNF-α are higher in patients with sleep apnea compared to normal controls, and decrease after only one month of CPAP treatment.TNF-α is a key regulator of insulin resistance and metabolic syndrome, and in vivo and ex vivo assays have demonstrated that TNF-α impairs insulin beacons and leads to disruption of insulin-mediated glucose uptake and storage, and that TNF-α is a key regulator of glucose metabolism in patients with sleep apnea. Inhibition of TNF-α can improve insulin sensitivity. In addition to TNF-α, IL-6 has been implicated as another cytokine in the pathogenesis of insulin resistance and type II diabetes. levels of IL-6 are high in patients with type II diabetes, and increased in patients who are insulin resistant or predisposed to type II diabetes, but the role of IL-6 in glucose metabolism disorders is still poorly understood. Adipokines: Adipocytes are subject to afferent signaling from several different sources, including the autonomic nervous system and the HPA axis, and are also the source of efferent signaling, including leptin, TNF-α, IL-6, adiponectin, and resistin. Leptin, the protein product encoded by the obesity gene (ob gene), is a 167 amino acid endogenous hormone with a molecular weight of 16 kD, located mainly in adipocytes, but also seen in the stomach and skeletal muscle, and its plasma concentration is mainly related to overall adipocyte volume, which is also stimulated by hypoxemia. In addition to its central role in regulating energy expenditure and food intake through hypothalamic actions and its role in the central nervous system as an appetite suppressant, leptin also has a wide range of peripheral effects on physiological processes that regulate glucose homeostasis. Studies have shown that leptin improves insulin sensitivity in peripheral tissues, and the leptin-mediated reduction in insulin secretion and improvement in insulin sensitivity may explain the hyperinsulinemia and insulin resistance in leptin-deficient ob/ob rats. However, the role of leptin in the clinical state is much more complex, as leptin levels are elevated in the majority of obese patients, which makes it easy to envision a possible correlation between insulin resistance and leptin resistance in obese patients. Studies have demonstrated that leptin levels are also markedly elevated in typically obese OSAHS patients and are higher than in patients who are also obese but do not have OSAHS, and that leptin levels are similarly elevated in nonobese OSAHS patients.Hyperleptinemia in OSAHS may indicate that the target tissues are resistant to the weight-reducing effects of leptin. The mechanisms that lead to increased leptin levels in OSAHS are not clear. Studies have confirmed that AHI does not have an additive effect on leptin levels, suggesting that elevated leptin levels in OSAHS may be related to its higher visceral adiposity and/or cytokines, and that leptin itself is an inflammation-inducing factor. Effects of sleep apnea treatment on glucose metabolism The current standard treatment for OSAHS is nasal Continuous Positive Airway Pressure (nCPAP), which involves applying a lower positive pressure (usually 4-10 cm H2O) to the patient’s airway through a nasal mask while the patient sleeps thus preventing the collapse of the upper airway. This safe and simple treatment provides rapid relief of daytime sleepiness and improves the patient’s general condition. Many studies have clearly demonstrated that effective treatment of OSAHS can improve cardiovascular risk factors and impaired cardiac function. In recent years, many studies have also investigated the changes in glucose metabolism in OSAHS patients before and after CPAP therapy, but the results were not consistent because the duration of CPAP therapy and the original situation were not the same in each study, and most of the studies had the drawbacks of not having a control group, too small a sample size to be statistically persuasive, and a lack of data on the adherence to CPAP therapy, and therefore, some of them failed to detect the effect of CPAP treatment on glucose metabolism is not surprising. One of the studies with the largest sample size demonstrated that insulin sensitivity improved significantly after two days of effective CPAP treatment and continued to be maintained after three months of continuous CPAP treatment, even though there was no significant change in body weight during this period. These results suggest that insulin resistance is a feature of OSAHS itself, and that insulin resistance can be improved by CPAP therapy. Obesity is an important modifier of treatment outcome, and studies have shown that insulin sensitivity improves more rapidly in leaner patients and better in leaner patients than in obese patients at all time points in the treatment, thus obesity is a major predictor of insulin changes in CPAP therapy in patients with OSAHS. Most studies have reported that short-term (2-4 days) or long-term (3-6 months) effective CPAP therapy (even with an AHI <5/h) reduces blood leptin levels in patients with OSAHS independently of whether the patients lose weight or not, but that leptin levels remain high if the treatment is ineffective in patients with OSAHS.Ip et al. demonstrated that triglyceride levels in patients treated with CPAP are also reduced, but fasting insulin levels are not. reduced, but fasting insulin and glucose concentrations were not altered. Conclusion In summary, there is reason to believe that there is a potentially significant correlation between OSAHS and metabolic abnormalities, and although the causal relationship is unclear and there is a relative lack of evidence from which definitive conclusions can be drawn, there is a possibility that sleep apnea may be a precursor to negative metabolic consequences. When exploring the possible mechanisms by which OSAHS contributes to the increased incidence of cardiovascular disease, insulin resistance and the metabolic syndrome are among the most prominent possible causes, while other possible mediators include leptin, IL-6, and TNF-α. Effective CPAP therapy (either short- or long-term) can significantly improve the metabolic abnormalities in OSAHS, thereby decreasing cardiovascular disease incidence and improving the patient's Prognosis.