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Voluntary activity reverses spermidine-induced myocardial fibrosis and lipid accumulation in the obese male mouse
Histochemistry and Cell Biology ( IF 2.1 ) Pub Date : 2020-10-27 , DOI: 10.1007/s00418-020-01926-1
Christian Mühlfeld 1, 2 , Clara Pfeiffer 1 , Vanessa Schneider 1 , Melanie Bornemann 1 , Julia Schipke 1, 2
Affiliation  

Obesity due to high calorie intake induces cardiac hypertrophy and dysfunction, thus contributing to cardiovascular morbidity and mortality. Recent studies in aging suggest that oral supplementation with the natural polyamine spermidine has a cardioprotective effect. Here, the hypothesis was tested that spermidine or voluntary activity alone or in combination protect the heart from adverse effects induced by obesity. Therefore, C57Bl/6 mice (n = 8–10 per group) were subjected to control or high fat diet (HFD) and were left untreated, or either received spermidine via drinking water or were voluntarily active or both. After 30 weeks, the mice were killed and the left ventricle of the hearts was processed for light and electron microscopy. Design-based stereology was used to estimate parameters of hypertrophy, fibrosis, and lipid accumulation. HFD induced cardiac hypertrophy as demonstrated by higher volumes of the left ventricle, cardiomyocytes, interstitium, myofibrils and cardiomyocyte mitochondria. These changes were not influenced by spermidine or voluntary activity. HFD also induced myocardial fibrosis and accumulation of lipid droplets within cardiomyocytes. These HFD effects were enhanced in spermidine treated animals but not in voluntarily active mice. This was even the case in voluntarily active mice that received spermidine. In conclusion, the data confirm the induction of left ventricular hypertrophy by high-fat diet and suggest that—under high fat diet—spermidine enhances cardiomyocyte lipid accumulation and interstitial fibrosis which is counteracted by voluntary activity.



中文翻译:

肥胖雄性小鼠的自愿活动逆转了亚精胺诱导的心肌纤维化和脂质蓄积

由于高卡路里摄入引起的肥胖症会诱发心脏肥大和功能障碍,从而导致心血管疾病和死亡。关于衰老的最新研究表明,口服天然多胺亚精胺具有心脏保护作用。在此,对假说进行了检验,即单独或联合使用亚精胺或自愿活动可以保护心脏免受肥胖引起的不良影响。因此,C57Bl / 6小鼠(n = 8-10(每组))接受对照或高脂饮食(HFD),不予治疗,或者通过饮用水接受亚精胺治疗,或者自愿活动,或两者兼而有之。30周后,处死小鼠,并处理心脏的左心室以进行光镜和电子显微镜检查。基于设计的立体感用于估计肥大,纤维化和脂质堆积的参数。HFD引起的心肌肥大由左心室,心肌细胞,间质,肌原纤维和心肌线粒体的体积增加所证明。这些变化不受亚精胺或自愿活动的影响。HFD还诱导心肌纤维化和心肌细胞内脂质滴的积累。这些HFD效果在亚精胺治疗的动物中得到增强,但在自愿活动的小鼠中却没有得到增强。甚至在接受亚精胺的自愿活动小鼠中也是如此。总之,数据证实高脂饮食可诱发左心室肥大,并表明在高脂饮食下亚精胺可增强心肌脂质的蓄积和间质纤维化,而自愿性活动可抵消这种作用。

更新日期:2020-10-30
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