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首页> 外文期刊>Life sciences >Long-term high-fat diet-induced obesity decreases the cardiac leptin receptor without apparent lipotoxicity.
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Long-term high-fat diet-induced obesity decreases the cardiac leptin receptor without apparent lipotoxicity.

机译：长期高脂饮食诱导的肥胖症会降低心脏瘦素受体，而没有明显的脂毒性。

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AIMS: Leptin resistance has been associated with cardiac lipotoxicity; however, whether leptin resistance is a risk factor associated with cardiac lipotoxicity at different time points in diet-induced obesity is unclear. The objective of this study was to evaluate this relationship. MAIN METHODS: Male Wistar rats were fed a normal chow diet (12% from fat) or a high-fat diet (49% from fat) for 15 and 45 weeks, respectively. The adiposity index, body weight and co-morbidities were evaluated. Heart lipotoxicity was assessed by analyzing cardiac function and morphological changes as well as cardiac triglyceride, ceramide and lipid hydroperoxide accumulations. Cardiac apoptosis was examined using the TUNEL method. Leptin function was determined by examining plasma leptin levels, cardiac leptin receptors (OB-R) and related phosphorylations of AMP-activated kinase protein (AMPK) and Acetyl CoA carboxylase (ACC). KEY FINDINGS: The diet-induced obesity was characterized by an elevated adiposity index, body weight and leptin levels at both 15 and 45 weeks. There was no difference between groups in the cardiac triglyceride or lipid hydroperoxide levels. Interestingly, ceramide levels decreased in obese animals in both experimental periods. The cardiac morphological and functional parameters were not altered. Although down-regulation of OB-R has occurred in chronic obesity, it did not adversely affect AMPK or ACC phosphorylation. SIGNIFICANCE: The development of obesity via long-term feeding of a high-fat diet to rats does not result in cardiac lipotoxicity but promotes the down-regulation of OB-R. However, this does not result in altered levels of AMPK or ACC phosphorylations in this animal model.
机译：目的：瘦素抵抗与心脏脂质毒性有关。然而，在饮食诱导的肥胖的不同时间点，瘦素抵抗是否是与心脏脂质毒性相关的危险因素尚不清楚。这项研究的目的是评估这种关系。主要方法：雄性Wistar大鼠分别接受普通食物（脂肪含量的12％）或高脂饮食（脂肪含量的49％）持续15周和45周。评价肥胖指数，体重和合并症。通过分析心脏功能和形态变化以及心脏甘油三酸酯，神经酰胺和脂质过氧化氢的积累来评估心脏脂质毒性。使用TUNEL方法检查心脏凋亡。瘦素功能通过检查血浆瘦素水平，心脏瘦素受体（OB-R）以及AMP激活激酶蛋白（AMPK）和乙酰CoA羧化酶（ACC）的相关磷酸化来确定。主要发现：饮食引起的肥胖症的特征是在15周和45周时，肥胖指数，体重和瘦素水平升高。两组之间的心脏甘油三酸酯或脂质氢过氧化物水平没有差异。有趣的是，在两个实验期间，肥胖动物的神经酰胺水平均下降。心脏的形态和功能参数没有改变。尽管在慢性肥胖症中发生了OB-R的下调，但它并未对AMPK或ACC磷酸化产生不利影响。意义：通过长期向大鼠饲喂高脂饮食来发展肥胖症不会导致心脏脂质毒性，但会促进OB-R的下调。但是，这不会导致该动物模型中AMPK或ACC磷酸化水平的改变。

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