Journal
FREE RADICAL RESEARCH
Volume 44, Issue 2, Pages 128-134Publisher
TAYLOR & FRANCIS LTD
DOI: 10.3109/10715760903348328
Keywords
Adiponectin; mTOR; reactive oxygen species; nitric oxide; AMPK
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Funding
- Ministry of Education, Culture, Sports, Science, and Technology of Japan [20592457]
- Grants-in-Aid for Scientific Research [20592457] Funding Source: KAKEN
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Globular adiponectin (gAd) induces the generation of reactive oxygen species (ROS) and nitric oxide (NO) in the murine macrophage cell line RAW 264. This study investigated the role of the mammalian target of rapamycin (mTOR) in gAd-induced ROS and NO generation. gAd stimulation induced phosphorylation of mTOR, which peaked at 20 min and dissolved rapidly. Inhibition of phosphatidylinositol 3-kinase activity with wortmannin suppressed gAd-induced phosphorylation of Akt and mTOR. Administration of rapamycin partially reduced gAd-induced generation of intracellular and mitochondrial ROS, but not release of NO. To further confirm the role of mTOR in gAd stimulation, the effect of the activators of AMP-activated protein kinase (AMPK) on gAd-induced mTOR phosphorylation was examined. Pre-treatment with three kinds of AMPK activators, AICAR, 2-deoxy-D-glucose and A-769662, suppressed gAd-induced mTOR phosphorylation. Furthermore, these AMPK activators significantly reduced gAd-evoked intracellular and mitochondrial ROS generation and NO release.
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