目的：探讨慢性胆囊炎患者血清瘦素（Lep）、可溶性瘦素受体（sLR）与血脂水平的变化及其相互关系。方法：选择103 例慢性胆囊炎患者，以91 例健康体检者为对照，测定所有受试者空腹血清Lep、sLR、总胆固醇（TC）、甘油三酯（TG）、低密度脂蛋白（LDL）、高密度脂蛋白（HDL），分析慢性胆囊炎患者血清Lep、sLR 水平与血脂水平的关系。结果：与对照组比较，慢性胆囊炎组患者血清TC、LDL 和Lep 水平均明显升高，而sLR 水平明显降低（均P<0.05）。单因素分析显示，Lep 水平与TC、TG 和HDL 水平呈明显正相关（均P<0.05），而sLR 水平与各血脂指标无明显相关性（均P>0.05）；多元回归分析显示，Lep 水平与TC 水平呈明显正相关（P<0.05）。结论：慢性胆囊炎患者血清Lep 明显升高、sLR 水平降低以及血脂代谢紊乱，其中，Lep 升高所致胆固醇代谢障碍可能是主要原因。
Alteration of leptin, soluble leptin receptor and blood lipid levels and their relations in patients with chronic cholecystitis
Objective: To investigate the changes of serum leptin (Lep) and soluble leptin receptor (sLR) levels as well as blood lipid profile and their reciprocal relationship in patients with chronic cholecystitis. Methods: One hundred and three patients with chronic cholecystitis were enrolled, and 91 individuals undergoing health maintenance examinations served as control. In all subjects, the fasting serum levels of Lep and sLR and blood lipid indicators that included total cholesterol (TC), triglyceride (TG), low-density lipoprotein (LDL) and high-density lipoprotein (HDL) were measured, and the relations of serum Lep and sLR levels with blood lipid parameters in chronic cholecystitis patients were also analyzed. Results: Compared with control group, the levels of Lep, TC and LDL in chronic cholecystitis patients were increased, while the sLR level was decreased significantly (all P<0.05). In chronic cholecystitis patients, univariate analysis showed significantly positive correlation of Lep level with either TC, TG or HDL level (all P<0.05), while sLR level had no significant correlation with any of the blood lipid indicators (all P>0.05); multivariate regression analysis revealed that there was a significantly positive correlation between Lep level and TC level (P<0.05). Conclusion: There are increased Lep level and decreased sLR level as were as lipid metabolism disorders in patients with chronic cholecystitis, in which the abnormal lipid metabolism caused by increased Lep level may play a causal role.