It has been shown that oleuropein, a phenolic compound in the fruit and leaves of the olive tree (Olea europaea) induces mammalian uncoupling protein 1 (UCP1) expression via an increased secretion of noradrenaline and adrenaline. This study investigated the effects of oleuropein on avian UCP (avUCP) expression as well as genes related to mitochondrial oxidative phosphorylation and biogenesis in cultured avian muscle cells, together with reactive oxygen species generation. Oleuropein induced avUCP as well as peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), nuclear respiratory factor-1 (NRF1), mitochondrial transcription factor A (TFAM) and ATP5a1 (a component of mitochondrial adenosine triphosphate synthase) gene expression and cytochrome c oxidase activity, indicating the induction of mitochondrial biogenesis. Sirtuin-1 (SIRT1) gene expression was also up-regulated by this compound, which could contribute to an increase in PGC-1α activity. Oleuropein suppressed the level of superoxide generation per mitochondrion, possibly via the up-regulation of avUCP and manganese superoxide dismutase (MnSOD) expression. Based on these findings, this study is the first to show that oleuropein may induce avUCP expression in avian muscle cells independent of the catecholamines, in which PGC-1α may be involved.

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This study investigated the intracellular mechanism governing the effects of oleuropein (OLE), a phenolic compound of Olea europaea, on mRNA expression of avian uncoupling protein (avUCP) and mitochondrial biogenesis-related factors, and reactive oxygen species (mitROS) generation in a primary cultured chicken muscle cells.The OLE-treated cells exhibited increases in Avucp and ATP5a1z expression and a decrease in mitROS generation (p < 0.05), while the effects was canceled by sirtuin-1 (SIRT1) or transient receptor potential vanilloid 1 (TRPV1) inhibitors, EX-527 or BCTC, respectively. Intracellular Ca 2+ concentration was significantly increased by OLE, while the induction was canceled by BCTC. The study also found that TRPV1 was expressed in the cell membrane and endoplasmic reticulum (ER), and Ca 2+ could be released from ER in the OLE-treated cells. The OLE-treated cells exhibited increases in the phosphorylation ratio of AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) protein content. EX-527 and BCTC inhibitors canceled the effects of OLE on p-AMPK ratio and PGC-1α content, while EX-527 SIRT did not change PGC-1α content. The results suggest that the OLE effects may be due to Ca 2+ release, possibly from TRPV1 at ER, and increased p-AMPK ratio, followed by SIRT1 activation and PGC-1α protein expression.

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