Laboratory of Physiology and Pharmacology, Faculty of Medicine, Université Libre de Bruxelles, 808, Lennik Road, 1070, Brussels, Belgium.
Team of Cellular and Molecular Physiopathology, Faculty of Biological Sciences, Houari Boumediene University of Sciences and Technology, El Alia, Algiers, Algeria.
Lipids Health Dis. 2020 Jun 3;19(1):123. doi: 10.1186/s12944-020-01301-y.
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.
在代谢紊乱中，心肌脂肪浸润与脂肪毒性心肌病密切相关。
将 20 只沙鼠随机分为正常植物饮食组或高脂饮食组。16 周后，取心肌进行病理生物学评估。
16 周的高脂饮食导致心肌结构紊乱，伴有胶原沉积、脂质堆积、心肌细胞凋亡和炎症细胞浸润。心肌中葡萄糖转运蛋白 GLUT1 和丙酮酸脱氢酶（PDH）抑制剂 PDH 激酶（PDK）4 的表达增加，而胰岛素调节的 GLUT4 表达不变。调节脂肪酸转运的分子，如 CD36 和脂肪酸结合蛋白（FABP）3 的表达增加，而脂肪酸β氧化的限速酶肉碱棕榈酰转移酶（CPT）1B 的表达减少。心肌 AMP 激活蛋白激酶（AMPK）的表达减少，而过氧化物酶体增殖物激活受体（PPAR）-α 和 -γ 的表达没有变化。
在高脂饮食喂养的沙鼠中，一种具有遗传易感性和环境相互作用的营养诱导代谢综合征的原始实验模型，短期高脂喂养足以诱导心肌结构改变，并伴有心肌代谢基因表达的改变，有利于脂质堆积。
