CAJ | 학술논문

目的：探讨内质网应激（ ERS）在高脂饮食2型糖尿病转基因MKR小鼠脂肪肝发生中的作用。方法高脂饲料诱发MKR鼠形成脂肪肝，观察肝脏形态变化，检测肝脏甘油三酯和脂肪酸水平，RT－PCR检测小鼠肝脏内质网应激相关基因mRNA表达变化。结果与正常小鼠比较， MKR组小鼠肝脏GRP78、XBP1、FAS、ACC－α、GSK3βmRNA表达水平升高（P＜0．05）；与MKR小鼠比较，高脂饮食MKR小鼠肝脏甘油三酯（TG）和脂肪酸（FFA）水平显著升高（P＜0．01），肝脏GRP78、XBP1、CHOP、SREBP1c 、FAS、ACC－α、GSK3β和EDEM1基因mRNA表达水平均增加（P＜0．01），而ApoB100 mRNA表达水平降低（P＜0．01）。结论 ERS参与调节肝脏脂质及 ApoB100的代谢过程，在转基因2型糖尿病 MKR鼠脂肪肝形成中发挥重要作用。
목적：탐토내질망응격（ ERS）재고지음식2형당뇨병전기인MKR소서지방간발생중적작용。방법고지사료유발MKR서형성지방간，관찰간장형태변화，검측간장감유삼지화지방산수평，RT－PCR검측소서간장내질망응격상관기인mRNA표체변화。결과여정상소서비교， MKR조소서간장GRP78、XBP1、FAS、ACC－α、GSK3βmRNA표체수평승고（P＜0．05）；여MKR소서비교，고지음식MKR소서간장감유삼지（TG）화지방산（FFA）수평현저승고（P＜0．01），간장GRP78、XBP1、CHOP、SREBP1c 、FAS、ACC－α、GSK3β화EDEM1기인mRNA표체수평균증가（P＜0．01），이ApoB100 mRNA표체수평강저（P＜0．01）。결론 ERS삼여조절간장지질급 ApoB100적대사과정，재전기인2형당뇨병 MKR서지방간형성중발휘중요작용。
Objective To observe the effect of endoplasmic reticulum stress on the formation of liver steatosis in MKR mice raised by high fat feeds.Methods MKR mice were raised by high fat feeds to form liver steatosis.The pathological changes of liver were exam-ined,and the levels of TG and FFA in the liver were examined too.RT-PCR was used to analyze the related gene expressions of endoplasmic reticulum stress in the liver.Results The gene expressions of GRP78,XBP1,FAS,ACC-αand GSK3βon mRNA level in MKR mice were elevated slightly in contrast with normal mice(P<0.05).The levels of TG and FFA in the liver were increased remarkably,and the gene ex-pressions of GRP78,XBP1,CHOP,SREBP1c,FAS,ACC-α,GSK3βand EDEM1 on mRNA level in MKR mice with liver steatosis were ele-vated significantly in contrast with MKR mice(P<0.01),while the gene expression of apoB100 was decreased(P<0.01).Conclusions There has a close relationship between the liver steatosis and the involvement of ERS in the lipid metabolism in the liver of MKR mice.