摘要
目的探讨内脏脂肪微小RNA(mi R-152)表达的改变在高脂诱导胰岛素抵抗(IR)发病中的作用。方法实验分普通饲料(CN)组和高脂饮食诱导胰岛素抵抗(IR)两组;观察小鼠进食量和体质量,进行(IGTT)实验确定IR模型形成,测定空腹血糖(FBG)、空腹胰岛素(FINS)、血清胆固醇(TC)、甘油三酯(TG)和脂联素的含量,检测内脏脂肪mi RNA-152、过氧化物酶体增殖物激活受体(PPARγ,α)、脂肪细胞脂肪酸结合蛋白(a P2)、和胰岛素受体底物-1(IRS-1)基因表达的改变。结果 (1)两组小鼠喂养8w后进食量无明显改变,IR组体质量明显上升(P<0.05),内脏脂肪体质量比明显增加(P<0.05);(2)与CN组比较,IR组FBG无明显差异(P>0.05),INS显著升高(P<0.01),TC和TG明显上升(P<0.05),而脂联素含量明显降低(P<0.05);(3)IR较CN组小鼠内脏脂肪组织mi R-152表达明显下调(P<0.05),PPARγ和a P2基因表达明显增加(P<0.05),PPARα基因表达无差异,AKT和IRS-1基因表达明显下调(P<0.05);mi R-152表达仅与AKT基因表达呈正相关,与上述其他指标无相关性。结论内脏脂肪组织mi RNA-152表达下调,直接影响AKT表达而不是PPAR信号通路,是高脂诱导IR的重要发病机制之一。
Objective To determine the expression of miR-152 in visceral fat of mice during the development of insulin resistance （IR） induced by obesity. Methods Control group （CN） was fed a regular diet and IR group was fed a high fat diet. Body weight and food intake were recorded. IGTT experiment was used in the IR model development. The fasting blood glucose （FBG）, fasting insulin （FINS）, serum total cholesterol （TC）, triglycerides （TG） and adiponectin were detected, and the expressions of miRNA-152, peroxisome proliferator-activated receptor gamma （PPAR-γ）, adipocyte fatty acid binding protein （aP2）, PPAR-α, protein kinase B （AKT） and insulin receptor substrate （IRS-1） were determined. Results （1） After 8 weeks of feeding, body weight and visceral fat weight of IR mice were increased dramatically. However, there was no significant difference in food intake between IR group and control group. （2） Compared with the the CN group, the levels of INS, TC and TG were significantly increased in the IR group （P〈0.05）, while the content of adiponectin was decreased in the IR group （P〈0.05）. （3） Compared with the CN group, the expression of miR-152, as well as AKT and IRS-1 in visceral fat were downregulated in the the IR group （P 〈0.05）. On the contrary, PPARγ and aP2 were significantly upregulated in the IR group. Moreover, the expression of miR-152 was positively correlated with AKT expression. Conclusion The decreased expression of miR-152 in the visceral fat of IR mice induced by obesity affected the expression of AKT but not PPAR, which is one of the mechanisms that contributes to the IR development.
作者
赵晓云
邵凯
杨银荣
冯一民
ZHAO Xiao-yun, SHAO Kai, YANG Yin-rong, FENG Yi-min(Laboratory Medicine Center of Qilu Hospital, Shandong University（Qingdao）, Qingdao266035, China)
出处
《营养学报》
CAS
CSCD
北大核心
2018年第1期42-46,共5页
Acta Nutrimenta Sinica
基金
山东省医药卫生科技发展计划(No.2014WS0130)
