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A high-fat diet induced NMRI mouse model of metabolic syndrome: focus on brain-derived neurotrophic factor (BDNF)

机译:一种高脂饮食诱导的代谢综合征NMRI小鼠模型:专注于脑源性神经营养因子(BDNF)

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The association of brain-derived neurotrophic factor (BDNF) as a member of neurotrophin family and metabolic syndrome (MetS) has been proposed, however basic evidence necessary to prove (or disprove) this association in non-genetic animal model is rare. Therefore, we investigated the alteration of encephalic BDNF gene expression in a mouse model of high-fat diet (HFD) induced MetS. To translate MetS, male NMRI mice (9 weeks old; N = 13) fed on a HFD including suet powder (37.50%) and granulated sugar (19.85%) while control mice were fed a diet contained suet powder (6.25%) and granulated sugar (49.09%). We monitored the development of MetS by measuring fasting blood sugar (FBS) and lipid (total cholesterol (TC) and triacylglycerol (TGs)) and lipoprotein (high-density lipoprotein cholesterol (HDL-C), very low-density lipoprotein cholesterol (VLDL-C)) profiles, atherogenic index (AI), and somatic indices after 1 and 3 months of dietary interventions. The HFD intake led to increased body weight, liver weight, FBS, TC, and decreased HDL-C as compared to chow diet in mice after first month of dietary intervention. The increased FBS, body weight, abdominal fat mass, TGs, TC, and VLDL-C and decreased HDL-C were observed in HFD-fed mice as compared to those of chow-fed mice at 3th month. The statistical comparison of two HFD groups in two time intervals of 1st and 3th month confirmed that our HFD-induced MetS model was reliable because FBS, TGs and VLDL-C, TC, and AI have been increased significantly during selected time intervals. The AI increased significantly in HFD-fed mice compared to chow-fed mice after 3 months. The AI in HFD-fed mice treated with HFD for 3 months was increased significantly as compared to mice fed HFD for 1 month. Our diet-induced model more closely mimics the changes observed in human MetS and showed that encephalic BDNF gene in mice fed HFD was under-expressed by 0.30 fold with respect to chow-fed mice after 3 months of dietary intervention.
机译:提出了脑衍生的神经营养因子(BDNF)作为神经营养素家族和代谢综合征(METS)的成员的关联,但证明(或反驳)在非遗传动物模型中的基本证据是罕见的。因此,我们研究了在高脂饮食(HFD)诱导的Mets的小鼠模型中脑BDNF基因表达的改变。转化Mets,雄性NMRI小鼠(9周龄; N = 13)在包括Suet粉末(37.50%)和砂糖(19.85%),而对照小鼠喂食饮食含有Suet粉末(6.25%)并造粒糖(49.09%)。我们通过测量空腹血糖(FBS)和脂质(总胆固醇(TC)和三酰基甘油(TGS))和脂蛋白(高密度脂蛋白胆固醇(HDL-C),非常低密度脂蛋白胆固醇(VLDL)来监测METS的开发-C))饮食干预后1和3个月后的细胞生殖指数(AI)和体细胞义数。在膳食干预后,与小鼠中的饮食相比,HFD摄入量导致体重,肝脏重量,FBS,TC和降低的HDL-C。与第3个月的细胞饲料小鼠相比,在HFD-FED小鼠中观察到增加的FBS,体重,腹部脂肪物质,TGS,TC和VLDL-C和降低的HDL-C。两个HFD组在第1和第3个月的两次间隔的统计比较证实,我们的HFD诱导的METS模型是可靠的,因为在选定的时间间隔期间FBS,TGS和VLDL-C,TC和AI显着增加。与3个月后,与Chow Fed小鼠相比,AI在HFD喂养小鼠中显着增加。与喂养HFD的小鼠1个月相比,用HFD处理3个月处理3个月的HFD喂养小鼠中的AI显着增加。我们的饮食诱导的模型更加密切地模仿人体会科的变化,并显示喂养HFD小鼠的脑膜BDNF基因在膳食干预3个月后,喂养HFD的小鼠的表达0.30倍。

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