In metabolic disorders, myocardial fatty infiltration is critically associated with lipotoxic cardiomyopathy. Twenty Psammomys obesus gerbils were randomly assigned to normal plant or high fat diet. Sixteen weeks later, myocardium was sampled for pathobiological evaluation. A sixteen-week high fat diet resulted in myocardial structure disorganization, with collagen deposits, lipid accumulation, cardiomyocyte apoptosis and inflammatory cell infiltration. Myocardial expressions of glucose transporter GLUT1 and pyruvate dehydrogenase (PDH) inhibitor, PDH kinase (PDK)4 increased, while insulin-regulated GLUT4 expression remained unchanged. Myocardial expressions of molecules regulating fatty acid transport, CD36 and fatty acid binding protein (FABP)3, were increased, while expression of rate-controlling fatty acid β-oxidation, carnitine palmitoyl transferase (CPT)1B decreased. Myocardial expression of AMP-activated protein kinase (AMPK), decreased, while expression of peroxisome proliferator activated receptors (PPAR)-α and -γ did not change. In high fat diet fed Psammomys obesus, an original experimental model of nutritionally induced metabolic syndrome mixing genetic predisposition and environment interactions, a short period of high fat feeding was sufficient to induce myocardial structural alterations, associated with altered myocardial metabolic gene expression in favor of lipid accumulation.

中文翻译：

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高脂饮食改变了沙鼠沙鼠的心脏代谢基因谱。

在代谢疾病中，心肌脂肪浸润与脂毒性心肌病至关重要。将二十只沙鼠沙鼠随机分配到正常植物或高脂饮食中。十六周后，取心肌进行病理生物学评估。十六周的高脂饮食导致心肌结构紊乱，胶原蛋白沉积，脂质积聚，心肌细胞凋亡和炎性细胞浸润。葡萄糖转运蛋白GLUT1和丙酮酸脱氢酶（PDH）抑制剂PDH激酶（PDK）4的心肌表达增加，而胰岛素调节的GLUT4表达则保持不变。调节脂肪酸运输的分子CD36和脂肪酸结合蛋白（FABP）3的心肌表达增加，而控制速率的脂肪酸β-氧化的心肌表达增加，肉碱棕榈酰转移酶（CPT）1B减少。心肌中AMP活化蛋白激酶（AMPK）的表达下降，而过氧化物酶体增殖物激活受体（PPAR）-α和-γ的表达未改变。在高脂饮食喂养的Psammomys obesus中，这是一种营养诱发的代谢综合征的原始实验模型，混合了遗传易感性和环境相互作用，短时间的高脂喂养足以诱导心肌结构改变，并伴随着心肌代谢基因表达的改变而有利于脂质积累。