内科学
内分泌学
CD36
过剩4
β氧化
生物
肉碱棕榈酰转移酶I
安普克
肉碱
脂肪生成
过氧化物酶体
AMP活化蛋白激酶
脂肪酸合酶
脂质代谢
葡萄糖转运蛋白
蛋白激酶A
胰岛素
激酶
受体
医学
新陈代谢
生物化学
作者
Abdelhamid Sahraoui,Céline Dewachter,Grégory Vegh,Kathleen Mc Entee,Robert Naeije,S. Aouichat-Bouguerra,Laurence Dewachter
标识
DOI:10.1186/s12944-020-01301-y
摘要
Abstract Background In metabolic disorders, myocardial fatty infiltration is critically associated with lipotoxic cardiomyopathy. Methods Twenty Psammomys obesus gerbils were randomly assigned to normal plant or high fat diet. Sixteen weeks later, myocardium was sampled for pathobiological evaluation. Results 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. Conclusion 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.
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