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首页> 外文期刊>The Journal of Nutritional Biochemistry >Heart energy metabolism impairment in Western-diet induced obese mice.
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Heart energy metabolism impairment in Western-diet induced obese mice.

机译：西方饮食诱发的肥胖小鼠心脏能量代谢受损。

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摘要

Nutritional transition has contributed to growing obesity, mainly by changing eating habits of the population. The mechanisms by which diet-induced obesity leads to cardiac injury are not completely understood, but it is known that obesity is associated to impaired cardiac function and energy metabolism, increasing morbidity and mortality. Therefore, our study aimed to investigate the mechanisms underlying cardiac metabolism impairment related to Western diet-induced obesity. After weaning, male Swiss mice were fed a Western diet for 16 weeks in order to induce obesity. After this period, the content of proteins involved in heart energy metabolism GLUT1, cytosolic lysate and plasma membrane GLUT4, AMPK, pAMPK, IR beta , IRS-1, PGC-1 alpha , CPT1 and UCP2 was evaluated. Also, the oxidative phosphorylation of myocardial fibers was measured by high-resolution respirometry. Mice in the Western diet group (WG) presented altered biometric parameters compared to those in control group, including higher body weight, increased myocardial lipid deposition and glucose intolerance, which demonstrate the obesogenic role of Western diet. WG presented increased CPT1 and UCP2 contents and decreased IRS-1, plasma membrane GLUT4 and PGC-1 alpha contents. In addition, WG presented cardiac mitochondrial dysfunction and reduced biogenesis, demonstrating a lower capacity of carbohydrates and fatty acid oxidation and also decreased coupling between oxidative phosphorylation and adenosine triphosphate synthesis. Cardiac metabolism impairment related to Western diet-induced obesity is probably due to damaged myocardial oxidative capacity, reduced mitochondrial biogenesis and mitochondria uncoupling, which compromise the bioenergetic metabolism of heart.
机译：营养过渡主要是通过改变人们的饮食习惯来促进肥胖的增长。饮食引起的肥胖导致心脏损伤的机制尚不完全清楚，但众所周知，肥胖与心脏功能和能量代谢受损，发病率和死亡率增加有关。因此，我们的研究旨在探讨与西方饮食引起的肥胖有关的心脏代谢受损的潜在机制。断奶后，给雄性瑞士小鼠喂食西方饮食16周，以诱导肥胖。在此期间之后，评估了参与心脏能量代谢GLUT1，胞质裂解物和质膜GLUT4，AMPK，pAMPK，IR beta，IRS-1，PGC-1 alpha，CPT1和UCP2的蛋白质的含量。另外，通过高分辨率呼​​吸测定法测量了心肌纤维的氧化磷酸化。与对照组相比，西方饮食组（WG）的小鼠的生物特征参数发生了变化，包括体重增加，心肌脂质沉积增加和葡萄糖耐量下降，这证明了西方饮食的致肥胖作用。工作组表示CPT1和UCP2含量增加，而IRS-1，质膜GLUT4和PGC-1α含量下降。此外，WG表现出心脏线粒体功能障碍和生物发生减少，表明碳水化合物和脂肪酸氧化的能力较低，并且氧化磷酸化与三磷酸腺苷合成之间的偶联也降低。与西方饮食引起的肥胖有关的心脏代谢障碍可能是由于心肌氧化能力受损，线粒体生物发生减少和线粒体解偶联，这损害了心脏的生物能代谢。

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