非酒精性脂肪性肝病中抵抗素和肝纤维化的关系

目的：初步探讨非酒精性脂肪性肝病患者血清中抵抗素和肝脏纤维化之间关系。方法同期于本院体检科随机抽取非酒精性脂肪性肝病（NAFLD）病例共70例，健康体检者74例作正常对照组，比较两组研究对象的体质量指数（BMI）、腰臀比、空腹血糖（ FBG）、空腹胰岛素、糖化血红蛋白（ HbA1c）、血脂、胰岛素抵抗指数（ HOMA-IR）、肝酶、透明质酸、IV胶原、抵抗素、白介素-18（ IL-18）。结果 NAFLD组与正常对照组相比，收缩压、BMI、腰臀比、甘油三酯、HOMA-IR、ALT、AST、透明质酸、IV胶原、抵抗素、IL-18均升高，差异有统计学意义（ P ＜0.05），抵抗素与腰臀比、BMI、ALT、HOMA-IR、TG、IV胶原、IL-18呈正相关（ r ＝0.231，0.341，0.223，0.264，0.213，0.315，0.669， P ＜0.05），偏相关分析可见，抵抗素和ALT、IV胶原相关（ r ＝0.222，0.326， P ＜0.05）。结论抵抗素可能通过促进胰岛素抵抗及炎症反应来参与NAFLD的发生和发展。

Relations between resistin and hepatic fibrosis in nonalcoholic fatty liver disease subjects

Objective To evaluate the relationship between resistin and hepatic fibrosis in nonalcoholic fatty liver disease （NAFLD） subjects.Methods Serum resitin and Interleukin （IL）-18＆#39;s concentrations were measured in 144 subjects （70 NAFLD pa-tients and 74 healthy controls） with enzyme-linked immunosorbent assay （ELISA） and their serum alanine aminotransferase （ALT）, aspartate aminotransferase （AST）, fasting blood glucose （FBG）, HbA1c, triglyceride （TG）, total-cholesterol （TC）, low density lip-oprotein （ LDL） , high density lipoprotein （ HDL） , homeostasis model assessment of insulin resistance （ HOMA-IR） , hyaluronic acid , IVcollagen, height, body weight, waist circumference, and hip circumference were also measured .Their waist-to-hip ratio （WHR） and body mass indes （BMI） were calculated.Results There were higher levels of systolic blood pressure （SBP）, WHR, BMI, TG, ALT, AST, HOMA-IR, hyaluronic acid, IV collagen, resistin, and IL-18 in the NAFLD patients than those of the healthy controls （ P ＆lt;0.05 ） .The serum resistin level was significantly and positively correlated with WHR , BMI, ALT, HOMA-IR, TG, IV collagen , and IL-18 （ r =0.231 , 0.341 , 0.223 , 0.264 , 0.213 , 0.315 , and 0.669 , P ＆lt;0.05 ） .After adjustment for body fat and IL-18 , the serum resistin level was still significantly and positively correlated with ALT and IV collagen （ r =0.222 , 0.0.326 , P ＆lt;0.05 ） . Conclusions Resistin might take part in the development of NAFLD insulin resistance and its pro -inflammation.