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Chuck Reynolds
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What does Resveratrol induce.? P-9, P-1

Published on 6/18/2019
For additional information  Click Here

Resveratrol induces autophagy by directly inhibiting mTOR through ATP competition P-9


We demonstrated that mTOR is the direct target of resveratrol. This claim is supported by the observation that mTOR activity is inhibited by addition of resveratrol in vitro. Additionally, this study provides a mechanistic explanation for the beneficial effects of resveratrol, which is mTOR-dependent autophagy induction and reduction of cancer cell viability. These findings also increase the possibility of application of resveratrol to maladies that are highly associated with active mTOR, such as neurodegenerative diseases and diabetes.

Because of its beneficial effects, many researchers have attempted to identify the molecular target of resveratrol. SIRT1, a NAD+-dependent deacetylase, was initially identified as the direct target of resveratrol by in vitro screening. Additionally, other studies showed that the administration of resveratrol to mice and cells decreased the acetylation level of SIRT1 targets. The similarity in the functional outcome of SIRT1 activation and resveratrol administration suggested that SIRT1 can be a direct physiological target of resveratrol. However, several later studies reported that resveratrol did not activate SIRT1 in in vitro assays when native peptides, not fluorophore-tagged peptides (used in the original in vitro assay), were used as substrates.

These results suggested that SIRT1 may not be the direct target of resveratrol, although resveratrol clearly activates SIRT1 in vivo. Resveratrol was reported to activate AMPK (AMP-activated kinase) and additional studies have suggested that AMPK activation mediates the beneficial effects of resveratrol administration. Although resveratrol activates AMPK, AMPK is unlikely to be a direct target of resveratrol. After a long search for a direct target of resveratrol, Park et al. suggested PDEs (phosphodiesterases) as a direct target of resveratrol. In their report, they found that resveratrol inhibits PDEs through competition with cAMP (cyclic AMP), a substrate of PDE.

They also observed that inhibition of PDE is enough to mimic the effects of resveratrol administration in mice, such as AMPK activation, SIRT1 inhibition, and enhancement of metabolic features. Since the above-mentioned molecules are the known upstream regulators of mTORC1, inhibition of mTOR by resveratrol was thought to be due to these upstream regulators. However, we found that mTOR inhibition by resveratrol is independent of AMPK, SIRT1, PDE, and PI3K (data not shown).

Article Produced By
Department of Life Sciences, Pohang University of Science and Technology, Pohang 790-784, Republic of Korea
School of Interdisciplinary Bioscience and Bioengineering, Pohang University of Science and Technology, Pohang 790-784, Republic of Korea
School of Life Sciences, Ulsan National Institute of Science and Technology, Ulsan 689-798, Republic of Korea
Department of Bioscience and Biotechnology, Sejong University, 98 Kunja-Dong, Kwangjin-Ku, Seoul 143-747, Republic of Korea

(All these Articles can be read with this URL: )

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Chuck Reynolds

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