Endoplasmic Reticulum Stress Is Involved in Hepatic SREBP-1c Activation and Lipid Accumulation in Fructose-Fed Mice
会议名称：《中华预防医学会自由基预防医学专业委员会2012年夏季学术交流会》
会议日期：2012年
学科分类：1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学]
关 键 词：Fructose endoplasmic reticulum stress phenylbutyric acid hepatic lipid accumulation sterol regulatory element-binding protein
摘 要：A link between fructose drinking and nonalcoholic fatty liver disease(NAFLD) has been demonstrated in human and rodent *** aim of the present study was to investigate whether endoplasmic reticulum(ER)stress is mediated in the development of fructose-induced *** CD-I mice were fed with 30%fructose solution for eight *** lipid accumulation was *** nuclear sterol regulatory element-binding protein(SREBP)-lc was *** showed that hepatic SREBP-1c was activated in mice fed with fructose *** acid synthase(fas)and acetyl-CoA carboxylase(ace),two target genes of SREBP-lc,were ***-evoked hepatic SREBP-lc activation seemed to be associated with insulin-induced gene(Insig)-l *** ER stress and unfolded protein response(UPR),as determined by an increased glucose-regulated protein(GRP78)expression and an increased eIF2a and PERK phosphorylation,were observed in liver of mice fed with fructose *** acid(PBA),an ER chemical chaperone,not only significantly attenuated ER stress,but also alleviated fructose-induced hepatic Insig-1 *** inhibited fructose-evoked hepatic SREBP-lc activation and the expression of SREBP-lc target genes,and protected against hepatic lipid *** conclusion,ER stress contributes,at least in part,to hepatic SREBP-lc activation and lipid accumulation in fructose-evoked NAFLD.