肥胖致OSAHS发病新机制：内脏脂肪素对上气道肌群肌纤维蛋白分化的调节及相关通路研究

肥胖是OSAHS的独立危险因素，其发病机制长期以来被认为是机械因素为之。内脏脂肪素（visfatin）作为一种重要的脂肪因子，与内脏脂肪分布显著相关，且与肌肉代谢相关。我们前期研究证实OSAHS患者visfatin水平与AHI正相关。体外实验也初步发现visfatin对I型肌纤维蛋白具有抑制作用。因此推测肥胖者易患OSAHS可能与脂肪因子对颏舌肌结构和功能的影响有关。另有研究报道，活化的MAPK p38α/β是骨骼肌肌纤维蛋白分化和转换的关键通路，但visfatin是否通过此通路发挥作用尚无研究。因此本研究拟通过体外和体内实验，探讨visfatin对颏舌肌结构和功能的影响及相关机制，从新视角探讨肥胖致OSAHS的发病机制，为开拓OSAHS治疗新领域提供理论基础。

Obesity is a major but reversible independent risk factor for obstructive sleep apnea (OSA). Nowadays, most studies focus on the adipose's mechanical load in facilitating OSA, such as increases in neck circumference, narrowing of the upper airway (UA), etc.It is recognized that adipose tissue releasing a variety of adipokines is itself an endocrine organ.These adipokines are involved in metabolism, inflammation, energy homeostasis and development of obesity-related complications.But, whether and how adipokines could affect OSA is not well studied yet. . Visfatin, a new discovered protein adipokine, had the characteristic of mimic-insulin effect. It was predominantly secreted from visceral adipose tissue both in humans and mice. Our previous study showed that visfatin is strongly correlated with the severity of OSAHS, and high level may perform a negative effect on skeletal muscle I/II fiber synthesis.Besides, the p38 α/βis an essential pathway for skeletal muscle protein synthesis. Therefore, we investigate whether visfatin could affect upper airway muscle fiber via P38 α/βand accompaniment of skeletal muscle dysfunction.