脂肪肝患者肿瘤坏死因子-α与胰岛素抵抗的关系

来源 :中国基层医药 | 被引量 : 0次 | 上传用户:BecauseArc
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目的 探讨脂肪肝患者血清肿瘤坏死因子 α(TNF α)水平变化及其与胰岛素抵抗之间的关系。方法 用双抗体夹心ELISA法测定 5 7例脂肪肝患者 (其中肥胖组 32例 ,非肥胖组 2 5例 )及 4 0例正常对照组患者血清TNF α水平 ,同时测定体重指数 (BMI)、空腹血糖 (FPG)、空腹胰岛素 (FINS)、血脂 ,采用稳态模式(HOMA)评价胰岛素抵抗。结果 ①脂肪肝患者TNF α、BMI、FPG、FINS、HOMA、胆固醇 (TC)、甘油三脂(TG)、低密度脂蛋白 (LDL C)均高于对照组 (P <0 0 1,P <0 0 5 ) ,高密度脂蛋白 (HDL C)低于对照组 (P <0 0 5 )。②肥胖、非肥胖组脂肪肝TNF α、FPG、FINS、HOMA、TC、TG、LDL C均高于对照组 (P <0 0 1,P <0 0 5 ) ;肥胖组TNF α、BMI、FINS、HOMA、TG水平明显高于非肥胖组 (P <0 0 1,P <0 0 5 ) ;③脂肪肝患者TNF α与HOMA、BMI、FPG、FINS、TG呈正相关 ,多元线性回归分析显示 ,TNF α、FPG、TG是脂肪肝患者胰岛素抵抗的主要相关因素。结论 脂肪肝患者无论是否肥胖都存在胰岛素抵抗、血清TNF α水平升高 ,且TNF α在胰岛素抵抗的发病环节中起着重要的作用 Objective To investigate the changes of serum tumor necrosis factor α (TNF α) level and its relationship with insulin resistance in patients with fatty liver. Methods Serum levels of TNFα in 57 patients with fatty liver (32 in obesity group and 25 in non-obese group) and 40 normal controls were measured by double antibody sandwich ELISA. Body mass index (BMI), fasting Blood glucose (FPG), fasting insulin (FINS), blood lipids, and homeostasis model (HOMA) were used to evaluate insulin resistance. Results ① The levels of TNFα, BMI, FPG, FINS, HOMA, TC, TG and LDL in patients with fatty liver were significantly higher than those in control group (P <0.01, P < 0 05), HDL C was lower than that of the control group (P 0 05). ②The levels of TNFα, FPG, FINS, HOMA, TC, TG and LDL C in fatty liver of obesity and non-obese group were higher than those in control group (P <0.01, P <0.05) , HOMA and TG levels were significantly higher than those in non-obese patients (P <0.01, P <0.05). ③There was a positive correlation between TNFα and HOMA, BMI, FPG, FINS and TG in patients with fatty liver. Multivariate linear regression analysis showed that, TNFα, FPG, TG are the main related factors of insulin resistance in patients with fatty liver. Conclusion Patients with fatty liver have insulin resistance regardless of whether they are obese or not, serum TNF α levels rise, and TNF α plays an important role in the pathogenesis of insulin resistance
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