非酒精性脂肪性肝病患者血清SFRP5水平与血脂相关性分析

Correlation between secreted frizzled-related protein 5 level and blood lipids in serum of patients with nonalcoholic fatty liver disease

目的探讨分泌型卷曲相关蛋白5(SFRP5)在非酒精性脂肪性肝病(NAFLD)患者血清中的表达水平及其与血脂等相关影响因素的关系。方法收集58例NAFLD患者作为实验组,从体检中心选取58名健康体检者作为对照组;采用ELISA法检测血清SFRP5水平,分析NAFLD患者中SFRP5与相关影响因素的相关性。结果与对照组比较,实验组的体质量指数(BMI)、收缩压(SBP)、舒张压(DBP)、糖化血红蛋白(HBA1c)、三酰甘油(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、载脂蛋白B(Apo B)、尿酸(UA)、谷丙转氨酶(ALT)、谷草转氨酶(AST)、γ-谷氨酰转移酶(γ-GGT)和SFRP5水平明显升高(P<0.05或P<0.01);Pearson相关分析显示,血清SFRP5与TC、高密度脂蛋白胆固醇(HDL-C)和Apo B呈负相关性(P<0.05或P<0.01);Spearman相关分析显示,血清SFRP5与肝脏脂肪变呈正相关性(P=0.029,r=0.287);多元线性回归显示,TC是SFRP5的独立影响因素。结论 SFRP5在NAFLD中升高且与肝脏脂肪变呈正相关,与TC呈负相关,提示在对抗肝脏脂肪沉积、代谢应激和胰岛素抵抗等方面存在急性或慢性代偿机制,可能参与延缓NAFLD的发展。

Objective To investigate the expression level of secreted frizzled-related protein 5 （SFRP5） in serum of patients with non-alcoholic fatty liver disease （NAFLD） and the correlation of SFRP5 and relevant influencing factors such as blood lipids. Methods A total of 58 patients with NAFLD were selected as subjects （experimental group） and 58 healthy people were selected from the Physical Examination Center as controls （control group）. ELISA was used to detect the serum SFRP5 level and the correlation of SFRP5 of patients with NAFLD and relevant influencing factors was analyzed. Results Compared with the control group, levels of BMI, SBP, DBP, HbAlc, TG, TC, LDL-C, ApoB, UA, ALT, AST, y-GGT, and SFRP5 of the experimental group were significantly higher （P 〈0.05 or P 〈0.01）. Pearson correlation analysis showed that serum SFRP5 level negatively correlated with TC, HDL-C, and Apo-B （ P 〈0.05 or P 〈0.01）. Spearman correlation analysis showed that the serum SFRP5 level positively correlated with the content of liver fatty （ P =0. 029, r =0. 287）. Multivariate linear regression analysis showed that TC was the independent influencing factor of SFRP5. Conclusion Serum SFRP5 level of patients with NAFLD increases and positively correlates with the content of liver fatty and negatively correlates with TC, which suggest that there are chronic or acute compensatory mechanisms for counteracting liver fat accumulation, metabolic stress, and insulin resistance, and may contribute to delaying the development of NAFLD.