中文摘要：

过氧化物酶体增殖物激活受体α（PPARα）主要在肝脏中表达,饥饿时能诱导β-氧化与生酮作用相关基因和成纤维化生长因子21（FGF21）表达,这在肝脏的饥饿代谢适应中起重要作用。饥饿与耐力训练时,骨骼肌中,过氧化物酶体增殖物激活受体δ（PPARδ）能诱导长链脂肪酸（LCFAs）氧化基因、叉头转录因子（FOXO1）及PPARδ共激活物α1（PGC1α）表达,其中,FOXO1和PGC1α能调控糖代谢与线粒体生物发生。脂肪细胞中,PPARγ能介导LCFAs调控能量代谢,活化的PPARγ能诱导与LCFAs转化为甘油三酯形式储存相关的基因表达。脂联素,PPARγ的另一靶基因,能维持脂肪细胞的胰岛素敏感性。本文就PPARs在LCFAs调控能量代谢中的作用做一综述。

英文摘要：

PPAR-alpha expressed primarily in liver is essential for metabolic adaptation to starvation by inducing genes for beta-oxidation and ketogenesis to increase the utility of LCFAs and fibroblast growth factor 21. PPAR-delta induces genes for LCFA oxidation during fasting and endurance exercise in skeletal muscle. PPAR-deha also regulates glucose metabolism and mitochondrial biogenesis by inducing FOXO1 and PGCl-alpha. PPAR-gamma can induces the pathways to store LCFAs as triglycerides in adipocytes . Adiponectin, another important target of PPAR-gamma may maintain insulin sensitivity between adipo- cytes. The present review summarize that PPARs mediate the regulation of energy metabolism by long- chain fatty acids.