1.1 Bidirectional Relationship between Obstructive sleep apnea and Diabetes
Cross-sectional studies have shown that the prevalence of type 2 diabetes in patients with OSA ranges from 15–30%, and the prevalence of elevated glucose and insulin resistance is significantly higher in OSA patients than in the healthy population, with a dose-dependent risk. The co-prevalence of OSA in patients with type 2 diabetes was found to be about 71%.Intermittent hypoxia and sleep fragmentation in patients with OSA have been found to be associated with dysglycemia, insulin resistance, and abnormal islet β-cell function.To date, there have been prospective studies looking at the prevalence of type 2 diabetes in OSA patients with a follow-up period of 3 to 16 years, with inconsistent results across studies after correction for confounders. Another cross-sectional study found that diabetic patients with OSA had worse glycemic control than those without OSA. Currently, about More than half of all diabetic patients worldwide may be affected by both diabetes and OSA. The possible consequence of this is that patients with combined OSA may not have effective glycemic control. The possible consequence is that patients with combined OSA may not have effective glycemic control. Based on the current clinical findings, we have observed a significant increase in the number of patients with OSA. Based on current clinical findings, we have observed a higher prevalence of diabetes in patients with OSA. However, it is not yet possible to conclude whether OSA will lead to the development of type 2 diabetes over time. However, it is not possible to conclude conclusively whether OSA leads to the development of type 2 diabetes over time. Future studies should focus on the development of type 2 diabetes using strict criteria and follow-up in larger populations. Future studies should focus on the relationship between OSA and diabetes using strict criteria and longer follow-up in larger populations. The relationship between OSA and diabetes should also be addressed.
A follow-up study  with an average follow-up of 67 months showed that the initial severity of OSA and its physiological consequences could predict the risk of subsequent diabetes in OSA patients, controlling for multiple confounding factors. The current study demonstrates a strong association between OSA and insulin resistance, glucose intolerance and the risk of type 2 diabetes. And OSA is independently associated with poor glycemic control. A study of the association between OSA and diabetes showed that OSA patients have a higher BMI than patients with other conditions, and OSA is associated with endocrine diseases, especially diabetes[12–13] ..
1.2 Two-way mechanism between Obstructive sleep apnea and Diabetes
Results of prospective cross-sectional studies in indicating an independent association between OSA severity and insulin resistance in patients without type 2 diabetes, and short-term lab-based studies in healthy human subjects have demonstrated that sleep restriction, sleep fragmentation and intermittent hypoxemia can lead to glucose metabolism disorders.
In OSA, increased energy expenditure due to the increase of resting metabolic rate may induce compensatory neuroendocrine adaptation to increase hunger and food intake beyond energy balance requirements, leading to excess energy and a higher risk of obesity, leading to dyslipidemia, inflammatory status, and lower insulin sensitivity. The specific pathophysiological mechanisms are shown below:
(1) Increased sympathetic activity: Patients with OSA have increased sympathetic nerve activity, and intermittent hypoxemia and sleep structural disorders during sleep further stimulate sympathetic nerves leading to greater blood glucose fluctuations and insulin resistance , while hyperinsulinemia causes excessive stimulation of the carotid body, leading to increased sympathetic adrenal activity and blood flow, forming a vicious circle and exacerbating abnormal glucose metabolism .
(2) Intermittent hypoxia: Intermittent hypoxemia affects insulin sensitivity and impairs β-cell function, causing increased hepatic glycogen output and pancreatic oxygenation stress, which can increase fasting glucose levels by 67% and decrease glucose tolerance by 27%; even after correction of hypoxia, impaired glucose tolerance, insulin resistance and pancreatic β-cell function persist .
(3) Hypothalamic-pituitary-adrenal (HPA) axis dysfunction: Increased sympathetic nerve activity in OSA patients can activate the hypothalamic-pituitary-adrenal axis, resulting in increased glucocorticoid secretion. Glucocorticoid can promote glucose synthesis and glycogen decomposition, leading to insulin resistance.
(4) Systemic inflammatory response syndrome: This includes the release of pro-inflammatory mediators such as TNF -αand interleukin-6. The researchers also found elevated circulating levels of C-reactive protein, reactive oxygen species and advanced glycation end products in OSA patients.
(5) Changes in adipocytokines, such as increased leptin levels and decreased adiponectin levels.
(6) Fatigue and lethargy caused by OSA can lead to decreased body activity and increase the risk of diabetes, which is another mechanism of OSA causing diabetes. Sleep deprivation can lead to insulin resistance.
Diabetic autonomic dysfunction is a risk factor for OSA. Diabetic patients with peripheral neuropathy, especially autonomic nerve dysfunction, have an increased risk of sleep and respiratory disorders .
Chronic hyperglycemia leads to structural damage and functional impairment of the divine meridian through oxidative stress, which leads to functional impairment of the divine meridian through impaired control function of the central axis of respiration, leading to sleep and sleep respiratory disorders .
On the other hand, diabetic autonomic neuropathy may aggravate the collapse of the upper respiratory tract, reduce the diameter of the upper respiratory tract, affect the reaction of the upper respiratory tract due to the destruction of the laryngeal dilator muscle, and increase the susceptibility to obstructing respiratory suspension sleep disorders induced by OSA or painful peripheral neuropathy .