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A metabolomic study of the PPARδ agonist GW501516 for enhancing running endurance in Kunming mice

机译:PPARδ激动剂GW501516增强昆明小鼠耐力的代谢组学研究

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摘要

Exercise can increase peroxisome proliferator-activated receptor-δ (PPARδ) expression in skeletal muscle. PPARδ regulates muscle metabolism and reprograms muscle fibre types to enhance running endurance. This study utilized metabolomic profiling to examine the effects of , a PPARδ agonist, on running endurance in mice. While training alone increased the exhaustive running performance, treatment enhanced running endurance and the proportion of succinate dehydrogenase (SDH)-positive muscle fibres in both trained and untrained mice. Furthermore, increased levels of intermediate metabolites and key enzymes in fatty acid oxidation pathways were observed following training and/or treatment. Training alone increased serum inositol, glucogenic amino acids, and branch chain amino acids. However, increased serum galactose and β-hydroxybutyrate, independent of training. Additionally, alone raised serum unsaturated fatty acid levels, especially polyunsaturated fatty acids, but levels increased even more when combined with training. These findings suggest that mechanisms behind enhanced running capacity are not identical for and training. Training increases energy availability by promoting catabolism of proteins, and gluconeogenesis, whereas enhances specific consumption of fatty acids and reducing glucose utilization.
机译:运动可以增加骨骼肌中过氧化物酶体增殖物激活受体-δ(PPARδ)的表达。 PPARδ调节肌肉代谢并重新编程肌肉纤维类型,以增强跑步耐力。这项研究利用代谢组学分析来研究PPARδ激动剂对小鼠耐力的影响。虽然单独训练可以提高力竭的跑步性能,但治疗可以增强训练和未训练小鼠的跑步耐力和琥珀酸脱氢酶(SDH)阳性肌纤维的比例。此外,在训练和/或治疗后,观察到脂肪酸氧化途径中的中间代谢物和关键酶的含量增加。单独训练会增加血清肌醇,生糖氨基酸和支链氨基酸。但是,血清半乳糖和β-羟基丁酸酯增加,与训练无关。此外,单独提高血清不饱和脂肪酸水平,尤其是多不饱和脂肪酸,但与训练结合后,其水平甚至增加更多。这些发现表明,增强的运行能力背后的机制与培训并不相同。训练通过促进蛋白质的分解代谢和糖异生来增加能量的可利用性,而增加脂肪酸的比消耗并减少葡萄糖的利用。

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