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首页> 外文期刊>American Journal of Physiology >Effects of chronic activation of peroxisome proliferator-activated receptor-alpha or high-fat feeding in a rat infarct model of heart failure.
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Effects of chronic activation of peroxisome proliferator-activated receptor-alpha or high-fat feeding in a rat infarct model of heart failure.

机译：过氧化物酶体增殖物激活受体-α或高脂喂养的慢性激活对心力衰竭大鼠梗塞模型的影响。

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Intracardiac accumulation of lipid and related intermediates (e.g., ceramide) is associated with cardiac dysfunction and may contribute to the progression of heart failure (HF). Overexpression of nuclear receptor peroxisome proliferator-activated receptor-alpha (PPARalpha) increases intramyocellular ceramide and left ventricular (LV) dysfunction. We tested the hypothesis that activation of fatty acid metabolism with fat feeding or a PPARalpha agonist increases myocardial triglyceride and/or ceramide and exacerbates LV dysfunction in HF. Rats with infarct-induced HF (n = 38) or sham-operated rats (n = 10) were either untreated (INF, n = 10), fed a high-fat diet (45% kcal fat, INF + Fat, n = 15), or fed the PPARalpha agonist fenofibrate (150 mg.kg(-1).day(-1), INF + Feno, n = 13) for 12 wk. LV ejection fraction was significantly reduced with HF (49 +/- 6%) compared with sham operated (86 +/- 2%) with no significant differences in ejection fraction (or other functional or hemodynamic measures) among the three infarcted groups. Treatment with the PPARalpha agonist resulted in LV hypertrophy (24% increase in LV/body mass ratio) and induced mRNAs encoding for PPARalpha-regulated genes, as well as protein expression and activity of medium chain acyl-CoA dehydrogenase (compared with INF and INF + Fat groups). Myocardial ceramide content was elevated in the INF group compared with sham-operated rats, with no further change in the INF + Fat or INF + Feno groups. Myocardial triglyceride was unaffected by infarction but increased in the INF + Fat group. In conclusion, LV dysfunction and dilation are not worsened despite upregulation of the fatty acid metabolic pathway and LV hypertrophy or accumulation of myocardial triglyceride in the rat infarct model of HF.
机译：心脏内脂质和相关中间体（例如神经酰胺）的蓄积与心脏功能障碍有关，并且可能导致心力衰竭（HF）的进展。核受体过氧化物酶体增殖物激活受体-α（PPARalpha）的过表达增加了肌内神经酰胺和左心室（LV）功能障碍。我们测试了以下假设：脂肪喂养或PPARalpha激动剂激活脂肪酸代谢会增加心肌甘油三酸酯和/或神经酰胺，并加剧HF中的LV功能障碍。梗死诱导的心力衰竭大鼠（n = 38）或假手术大鼠（n = 10）未经治疗（INF，n = 10），喂养高脂饮食（45％大卡脂肪，INF +脂肪，n = 15），或喂食PPARalpha激动剂非诺贝特（150 mg.kg（-1）.day（-1），INF + Feno，n = 13）12周。与假手术组（86 +/- 2％）相比，HF组左室射血分数显着降低（49 +/- 6％），在三个梗死组之间射血分数（或其他功能或血液动力学指标）无显着差异。用PPARalpha激动剂治疗导致左心室肥大（左心室/体重比增加24％）并诱导编码PPARalpha调节基因的mRNA，以及蛋白表达和中链酰基辅酶A脱氢酶的活性（与INF和INF相比） +脂肪组）。与假手术大鼠相比，INF组的心肌神经酰胺含量升高，而INF +脂肪或INF + Feno组的心肌神经酰胺含量没有进一步变化。心肌甘油三酸酯不受梗塞影响，但在INF +脂肪组中增加。总之，尽管HF的大鼠梗塞模型中脂肪酸代谢途径的上调和LV肥大或心肌甘油三酸酯的积累，但LV功能障碍和扩张并未加重。

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