睡眠障碍与脂肪因子分泌谱的交互：代谢功能障碍的新机制

Background Sleep disorders-including sleep deprivation, obstructive sleep apnea (OSA), and circadian rhythm disruption-and metabolic diseases such as obesity and type 2 diabetes represent major, interconnected public health challenges. This review aims to synthesize current evidence on the bidirectional crosstalk between these conditions, with a focus on the mediating role of dysregulated adipokine secretion. Discussion We elaborate a mechanistic framework wherein specific sleep disturbances disrupt circadian rhythms and alter the secretory profiles of key adipokines, including leptin, adiponectin, interleukin-6 (IL-6), and angiopoietin-like protein 4 (ANGPTL4). Sleep deprivation and fragmentation promote a state of leptin dysregulation and reduce adiponectin levels, while OSA-driven intermittent hypoxia potently upregulates IL-6 and ANGPTL4. These alterations collectively contribute to insulin resistance, dyslipidemia, and chronic low-grade inflammation, thereby elevating metabolic disease risk. Conversely, obesity and diabetes exacerbate sleep disorders through pathways involving visceral adiposity, neuroendocrine dysfunction (e.g. HPA-axis activation), and diabetes-related symptoms (e.g. nocturia, neuropathic pain), forming a vicious cycle. Clinical and preclinical evidence underscores that the synchronization of sleep-circadian biology is fundamental to maintaining adipokine homeostasis and metabolic health. Conclusion The evidence positions sleep and circadian health as critical, modifiable determinants of metabolic risk. Integrating sleep assessment and evidence-based interventions (e.g. CPAP for OSA, sleep extension, circadian realignment) into standard preventive and clinical frameworks for metabolic diseases is a promising strategy. Public health initiatives should elevate 'quality sleep' as a pillar of health alongside nutrition and physical activity to mitigate the intertwined epidemics of metabolic and sleep disorders.