Stimulation of AMPK and enhancement of glucose uptake in muscle cells by quercetin and quercetin glycosides, the actives principles of Vaccinium vitis-idaea

Eid, Hoda M.; Martineau, LC; Saleem, Ammar; Asim, Mohammad; Vallerand, Diane; Benhaddou-Andaloussi, Ali; L, Nestor; Afshar, Ahmadreza; Arnason, J. T.; Haddad, Peter

doi:10.1055/s-0029-1234720

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“…High glucose-induced oxidative stress is linked to mitochondrial dysfunction, insulin resistance and metabolic syndrome [57]. Quercetin is thought to have a beneficial effect in various aspects of these metabolic diseases [20,25,31,32,58], either through restriction of ROS generation locally, or enhancement of cellular oxidative defences [34, [59][60][61][62]. Mechanisms of quercetin action have been reviewed [20] and it is apparent that information in the high glucose environment, and on longer term metabolic effects, remains limited.…”

Section: Discussionmentioning

confidence: 99%

Quercetin preserves redox status and stimulates mitochondrial function in metabolically-stressed HepG2 cells

Houghton

Kerimi

Tumova

et al. 2018

Free Radical Biology and Medicine

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ReuseThis article is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs (CC BY-NC-ND) licence. This licence only allows you to download this work and share it with others as long as you credit the authors, but you can't change the article in any way or use it commercially. More information and the full terms of the licence here: https://creativecommons.org/licenses/ TakedownIf you consider content in White Rose Research Online to be in breach of UK law, please notify us by emailing eprints@whiterose.ac.uk including the URL of the record and the reason for the withdrawal request. AbstractHyperglycemia augments formation of intracellular reactive oxygen species (ROS) with associated mitochondrial damage and increased risk of insulin resistance in type 2 diabetes. We examined whether quercetin could reverse chronic high glucose-induced oxidative stress and mitochondrial dysfunction. Following long-term high glucose treatment, complex I activity was significantly decreased in isolated mitochondria from HepG2 cells. Quercetin dose-dependently recovered complex I activity and lowered cellular ROS generation under both high and normal glucose conditions. Respirometry studies showed that quercetin could counteract the detrimental increase in inner mitochondrial membrane proton leakage resulting from high glucose while it increased oxidative respiration, despite a decrease in electron transfer system (ETS) capacity, and lower non-ETS oxygen consumption. A quercetin-stimulated increase in cellular NAD + /NADH was evident within 2 h and a two-fold increase in PGC-1 mRNA within 6 h, in both normal and high glucose conditions. A similar pattern was also found for the mRNA expression of the repulsive guidance molecule b (RGMB) and its long non-coding RNA (lncRNA) RGMB-AS1 with quercetin, indicating a potential change of the glycolytic phenotype and suppression of aberrant cellular growth which is characteristic of the HepG2 cells. Direct effects of quercetin on PGC-1 activity were minimal, as quercetin only weakly enhanced PGC-1 binding to PPAR in vitro at higher concentrations. Our results suggest that quercetin may protect mitochondrial function from high glucose-induced stress by increasing cellular NAD + /NADH and activation of PGC-1 -mediated pathways. Lower ROS in combination with improved complex I activity and ETS coupling efficiency under conditions of amplified oxidative stress could reinforce mitochondrial integrity and improve redox status, beneficial in certain metabolic diseases. Abbreviations oxygen species; ROXresidual oxygen consumption; SIRTsirtuin; TBP -TATA-box binding protein; TFAMmitochondrial transcription factor A; TR-FRETtime-resolved fluorescence energy transfer.Graphical Abstract:

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