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作 者:况洁 秦东璐 郭欣 陈瑾 唐晓禹 张天铧 于碧莲[1] KUANG Jie;QIN Donglu;GUO Xin;CHEN Jin;TANG Xiaoyu;ZHANG Tianhua;YU Bilian(Department of Cardiovascular Medicine,the Second Xiangya Hospital&Research Institute of Blood Lipid and Atherosclerosis,Central South University,Changsha,Hunan 410011,China)
机构地区:[1]中南大学湘雅二医院心血管内科中南大学血脂与动脉粥样硬化研究所,湖南省长沙市410011
出 处:《中国动脉硬化杂志》2022年第3期205-210,共6页Chinese Journal of Arteriosclerosis
基 金:国家自然科学基金资助项目(81670420);湖南省自然科学基金资助项目(2018JJ1045);中国心馨心血管健康基金会资助项目(2019-CCA-ACCESS-028)。
摘 要:目的探究载脂蛋白O(ApoO)基因敲除促进高脂饮食诱导的肥胖及代谢紊乱表现。方法将ApoO基因敲除杂合小鼠进行配种繁殖,提取子代小鼠的组织DNA,用PCR技术检测小鼠的基因型。实时荧光定量PCR和Western blot检测ApoO基因敲除mRNA和蛋白表达水平。饲喂高脂饮食后,通过小鼠体型、摄食量、肝脏脂质组学等观察小鼠代谢相关表型变化。结果成功繁殖并获得子代小鼠,高脂喂养后发现纯合小鼠出现肥胖,肝脏脂肪变性更加严重,肝脏脂质组学提示肝内甘油三酯聚集,磷脂组分发生改变。结论ApoO基因敲除促进高脂饮食诱导的肥胖及代谢紊乱,可能为代谢综合征和心血管疾病的防治提供新的作用靶点。Aim To investigate the effect of apolipoprotein O knockout mice promoting obesity and metabolic disorders challenged by high fat diet(HFD).Methods Breeding the ApoO heterozygous mice will get the homozygous mice offspring.PCR reaction was used to detect the gene genotype after extracting the mice tissue DNA.mRNA and protein expression of ApoO were determined by quantitative real-time PCR(qRT-PCR)and Western blot assay,respectively.After feeding with high-fat diet,the metabolic phenotypes in mice were observed by somatotype,food intake,lipidomic study in liver.Results The homozygous mice offspring were obtained.It was found that homozygous mice had obesity and more severe hepatic steatosis after HFD challenging.Lipidomics of the liver revealed obvious accumulation of triglyceride and significant changes of phospholipid components.Conclusion The deletion of ApoO may promote obesity and metabolic disorders induced by high-fat diet,which could provide a new target for the prevention and treatment of metabolic syndrome and cardiovascular diseases.
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