Exercise Laboratory, School of Physiology, Faculty of Health Science, University of Witwatersrand, Medical School, Johannesburg, South Africa.
Curr Opin Pharmacol. 2012 Jun;12(3):363-71. doi: 10.1016/j.coph.2012.02.008. Epub 2012 Mar 5.
Early animal, menstrual phase and gender comparative studies inconsistently support an oestrogen-induced increase in fat oxidation during exercise. Recent advances from studies of cellular signalling and gene expression provide evidence for inter-tissue and intramuscular mechanisms that demonstrate oestrogen's promotion of skeletal muscle fat oxidative capacity. Oestrogen or oestrogen-analogues act mainly through oestrogen receptor-alpha in skeletal muscle to stimulate the genomic expression of certain other nuclear hormone receptors and downstream targets to promote long chain fatty acid (LCFA) uptake, mitochondrial shuttling and β oxidation. Oestrogen increases the availability of LCFA substrate by enhancing adipocyte lipolysis and expression of genes promoting intramyocellular lipid storage. Oestrogen acts by non-genomic means to increase the activation of AMPK that may reinforce some direct genomic actions.
早期动物、月经周期和性别比较研究结果不一致，不能支持雌激素在运动中增加脂肪氧化。最近，细胞信号转导和基因表达研究的进展为组织间和肌内机制提供了证据，这些机制表明雌激素促进了骨骼肌的脂肪氧化能力。雌激素或雌激素类似物主要通过骨骼肌中的雌激素受体-α作用，刺激某些其他核激素受体和下游靶标的基因组表达，以促进长链脂肪酸（LCFA）的摄取、线粒体穿梭和β氧化。雌激素通过增强脂肪细胞脂解和促进肌内脂质储存的基因表达来增加 LCFA 底物的可用性。雌激素通过非基因组途径增加 AMPK 的激活，这可能增强一些直接的基因组作用。
