Arumugam Somasundaram, Sreedhar Remya, Thandavarayan Rajarajan A, Karuppagounder Vengadeshprabhu, Watanabe Kenichi
Department of Clinical Pharmacology, Niigata University of Pharmacy and Applied Life Sciences, 265-1, Higashijima, Akiha Ku, Niigata 956 8603, Japan.
Department of Clinical Pharmacology, Niigata University of Pharmacy and Applied Life Sciences, 265-1, Higashijima, Akiha Ku, Niigata 956 8603, Japan.
Drug Discov Today. 2016 Jun;21(6):1003-8. doi: 10.1016/j.drudis.2016.02.010. Epub 2016 Feb 22.
The energy substrate preference of the human heart is well regulated and is modified upon aging, in that the fetal heart uses glucose, whereas the adult heart utilizes fatty acids. Various human and animal studies suggest a shift in myocardial substrate utilization and decreased rate of myocardial fatty acid uptake and oxidation in heart failure. Given that fatty acids provide greater capacity for energy production compared with glucose, reverting the heart back to using fatty acids might be a therapeutic option for treating heart failure. Targeting the enzymes and/or genes responsible for, or controlling, fatty acid metabolism in the heart, such as peroxisome proliferator-activated receptors (PPARs), mitochondrial fatty acid metabolizing proteins, AMP-activated protein kinase (AMPK), and glucose transporters (GLUTs), could provide novel therapeutic insights for treating heart failure.
人类心脏的能量底物偏好受到良好调节，且会随着衰老而改变，胎儿心脏利用葡萄糖，而成人心脏利用脂肪酸。各种人类和动物研究表明，心力衰竭时心肌底物利用发生改变，心肌脂肪酸摄取和氧化速率降低。鉴于与葡萄糖相比，脂肪酸具有更大的能量产生能力，使心脏恢复使用脂肪酸可能是治疗心力衰竭的一种治疗选择。针对心脏中负责或控制脂肪酸代谢的酶和/或基因，如过氧化物酶体增殖物激活受体（PPARs）、线粒体脂肪酸代谢蛋白、AMP激活的蛋白激酶（AMPK）和葡萄糖转运蛋白（GLUTs），可能为治疗心力衰竭提供新的治疗思路。
