Increased cardiac fatty acid oxidation in a mouse model with decreased malonyl-CoA sensitivity of CPT1B

Mitochondrial fatty acid oxidation (FAO) is an important energy provider for cardiac work and changes in cardiac substrate preference are associated with different heart diseases. Carnitine palmitoyltransferase 1B (CPT1B) is thought to perform the rate limiting enzyme step in FAO and is inhibited by malonyl-CoA. The role of CPT1B in cardiac metabolism has been addressed by inhibiting or decreasing CPT1B protein or after modulation of tissue malonyl-CoA metabolism. We assessed the role of CPT1B malonyl-CoA sensitivity in cardiac metabolism. 13 samples from heart (4 WT, 4WT/E3A and 5 E3A/E3A) were analyzed

线粒体脂肪酸氧化（Mitochondrial fatty acid oxidation, FAO）是心脏做功的重要能量供给来源，心脏底物偏好的改变与各类心脏疾病密切相关。肉碱棕榈酰转移酶1B（Carnitine palmitoyltransferase 1B, CPT1B）被认为是FAO通路中的限速酶，其活性可被丙二酰辅酶A（malonyl-CoA）抑制。此前已有研究通过抑制或下调CPT1B蛋白，或是调控组织内丙二酰辅酶A代谢，对CPT1B在心脏代谢中的作用进行了探究。本研究评估了CPT1B的丙二酰辅酶A敏感性在心脏代谢中的作用。本次研究共分析了13例心脏样本，其中包含4例野生型（Wild Type, WT）、4例WT/E3A突变型以及5例E3A/E3A纯合突变型样本。