摘要
目的:分析在高脂饮食诱发大鼠非酒精性脂肪肝病(NAFLD)形成过程中胰岛素抵抗(IR)与IL-18之间的相关性,并探讨IL-18对大鼠NAFLD形成的作用.方法:将48只♂SD大鼠随机分为正常饮食组(NG)及高脂饮食组(FG),各24只,喂养至第2、4、6、8周末时,2组各随机抽取6只,抽取门静脉血测空腹血糖(FBS)、空腹胰岛素(FINS),计算空腹胰岛素抵抗指数(FIRI);检测血清及肝组织匀浆IL-18浓度;光镜检查肝组织切片以评价肝脏脂肪变性程度.结果:FG第4周末开始出现IR,血清及肝组织匀浆IL-18均随喂养时间的延长逐渐升高,各期均高于NG,肝组织匀浆IL-18在第2、4、6、8周末均与同期NG比较均有统计学差异均P<0.05),而血清IL-18是第4、6、8周末与同期NG比较均有统计学差异(均P<0.05).FINS、FIRI、血清及肝组织匀浆IL-18均与肝脂肪变性呈正相关(r=0.951,0.971,0.950,0.937,均P<0.05).血清IL-18与FINS、FIRI及肝组织匀浆IL-18与FINS、FIRI均成正相关(r=0.951,0.933,0.929,0.913,均P<0.05).结论:IR在高脂饮食诱发的NAFLD的发生发展中有重要作用,IL-18与IR形成有关,并与NAFLD的形成相关联.
AIM： To analyze the relationship between rats＇ degree of insulin resistance and the concentration of IL-18 during the process of developing nonalcoholic fatty liver disease （NAFLD） by feeding a fat-rich diet, and to discuss the effect of IL-18 on NAFLD in rats. METHODS： Forty-eight male SD rats were randomly divided into a normal diet group （NG） and a fat-rich diet group （FG）, and there were 24 rats in each group. At the end of feeding for 2, 4, 6 and 8 wk, 6 rats in each group were randomly selected, the serum fasting blood sugar （FBS）, fasting insulin （FINS） and the fasting insulin resistance index （FIRI）, and the concentration of IL-18 in serum and liver tissue serosity were measured. Hepatic steatosis in all rats was scored according to criteria under light microscopy. RESULTS： All FG rats had a significant elevated level of serum FINS, FIRI from the fourth weekend; The concentration of liver IL-18 and serum IL-18 of rats in FG was increasing gradually, in comparison with the NG, there was a difference in liver IL-18 of FG from the second weekend and serum IL-18 from the fourth weekend （all P 〈 0.05）. FINS, FIRI and IL-18 were all positively correlated with hepatic steatosis in FG （r = 0.951, 0.971, 0.950, 0.937, all P 〈 0.05）. Serum IL-18 and FINS, serum IL-18 and FIRI, liver IL-18 and FINS, liver IL-18 and FIRI all had positive relationship （r = 0.951, 0.933, 0.929, 0.913, all P 〈 0.05）. CONCLUSION： IR may play an important role in the development of NAFLD by feeding rats fat-rich diet, and IL-18 may participate in the pathogenesis of NAFLD possibly through with a link to IR.
出处
《世界华人消化杂志》
CAS
北大核心
2009年第17期1764-1767,共4页
World Chinese Journal of Digestology
基金
国家自然科学基金资助项目
No.30670945~~
