Glutaredoxins concomitant with optimal ROS activate AMPK through S-glutathionylation to improve glucose metabolism in type 2 diabetes.
Identifieur interne : 000454 ( Main/Exploration ); précédent : 000453; suivant : 000455Glutaredoxins concomitant with optimal ROS activate AMPK through S-glutathionylation to improve glucose metabolism in type 2 diabetes.
Auteurs : Kelei Dong [République populaire de Chine] ; Meiling Wu [République populaire de Chine] ; Xiaomin Liu [République populaire de Chine] ; Yanjie Huang [République populaire de Chine] ; Dongyang Zhang [République populaire de Chine] ; Yiting Wang [République populaire de Chine] ; Liang-Jun Yan [États-Unis] ; Dongyun Shi [République populaire de Chine]Source :
- Free radical biology & medicine [ 1873-4596 ] ; 2016.
Descripteurs français
- KwdFr :
- AMP-Activated Protein Kinases (génétique), AMP-Activated Protein Kinases (métabolisme), Alimentation riche en graisse (effets indésirables), Animaux (MeSH), Cellules HEK293 (MeSH), Cellules épithéliales (cytologie), Cellules épithéliales (métabolisme), Diabète de type 2 (anatomopathologie), Diabète de type 2 (métabolisme), Diabète expérimental (anatomopathologie), Diabète expérimental (métabolisme), Diabète expérimental (prévention et contrôle), Diabète expérimental (étiologie), Espèces réactives de l'oxygène (agonistes), Espèces réactives de l'oxygène (antagonistes et inhibiteurs), Espèces réactives de l'oxygène (métabolisme), Foie (anatomopathologie), Foie (métabolisme), Glucose (métabolisme), Glutarédoxines (génétique), Glutarédoxines (métabolisme), Glycogène (métabolisme), Humains (MeSH), Hépatocytes (cytologie), Hépatocytes (métabolisme), Lignée cellulaire (MeSH), Mâle (MeSH), Oxydoréduction (MeSH), Rat Sprague-Dawley (MeSH), Rats (MeSH), Régulation de l'expression des gènes (MeSH), Sous-unités de protéines (génétique), Sous-unités de protéines (métabolisme), Streptozocine (MeSH), Transduction du signal (MeSH).
- MESH :
- agonistes : Espèces réactives de l'oxygène.
- anatomopathologie : Diabète de type 2, Diabète expérimental, Foie.
- antagonistes et inhibiteurs : Espèces réactives de l'oxygène.
- cytologie : Cellules épithéliales, Hépatocytes.
- effets indésirables : Alimentation riche en graisse.
- génétique : AMP-Activated Protein Kinases, Glutarédoxines, Sous-unités de protéines.
- métabolisme : AMP-Activated Protein Kinases, Cellules épithéliales, Diabète de type 2, Diabète expérimental, Espèces réactives de l'oxygène, Foie, Glucose, Glutarédoxines, Glycogène, Hépatocytes, Sous-unités de protéines.
- prévention et contrôle : Diabète expérimental.
- étiologie : Diabète expérimental.
- Animaux, Cellules HEK293, Humains, Lignée cellulaire, Mâle, Oxydoréduction, Rat Sprague-Dawley, Rats, Régulation de l'expression des gènes, Streptozocine, Transduction du signal.
English descriptors
- KwdEn :
- AMP-Activated Protein Kinases (genetics), AMP-Activated Protein Kinases (metabolism), Animals (MeSH), Cell Line (MeSH), Diabetes Mellitus, Experimental (etiology), Diabetes Mellitus, Experimental (metabolism), Diabetes Mellitus, Experimental (pathology), Diabetes Mellitus, Experimental (prevention & control), Diabetes Mellitus, Type 2 (metabolism), Diabetes Mellitus, Type 2 (pathology), Diet, High-Fat (adverse effects), Epithelial Cells (cytology), Epithelial Cells (metabolism), Gene Expression Regulation (MeSH), Glucose (metabolism), Glutaredoxins (genetics), Glutaredoxins (metabolism), Glycogen (metabolism), HEK293 Cells (MeSH), Hepatocytes (cytology), Hepatocytes (metabolism), Humans (MeSH), Liver (metabolism), Liver (pathology), Male (MeSH), Oxidation-Reduction (MeSH), Protein Subunits (genetics), Protein Subunits (metabolism), Rats (MeSH), Rats, Sprague-Dawley (MeSH), Reactive Oxygen Species (agonists), Reactive Oxygen Species (antagonists & inhibitors), Reactive Oxygen Species (metabolism), Signal Transduction (MeSH), Streptozocin (MeSH).
- MESH :
- chemical , agonists : Reactive Oxygen Species.
- chemical , antagonists & inhibitors : Reactive Oxygen Species.
- chemical , genetics : AMP-Activated Protein Kinases, Glutaredoxins, Protein Subunits.
- chemical , metabolism : AMP-Activated Protein Kinases, Glucose, Glutaredoxins, Glycogen, Protein Subunits, Reactive Oxygen Species.
- adverse effects : Diet, High-Fat.
- cytology : Epithelial Cells, Hepatocytes.
- etiology : Diabetes Mellitus, Experimental.
- metabolism : Diabetes Mellitus, Experimental, Diabetes Mellitus, Type 2, Epithelial Cells, Hepatocytes, Liver.
- pathology : Diabetes Mellitus, Experimental, Diabetes Mellitus, Type 2, Liver.
- prevention & control : Diabetes Mellitus, Experimental.
- Animals, Cell Line, Gene Expression Regulation, HEK293 Cells, Humans, Male, Oxidation-Reduction, Rats, Rats, Sprague-Dawley, Signal Transduction, Streptozocin.
Abstract
AMPK dysregulation contributes to the onset and development of type 2 diabetes (T2DM). AMPK is known to be activated by reactive oxygen species (ROS) and antioxidant interference. However the mechanism by which redox state mediates such contradictory result remains largely unknown. Here we used streptozotocin-high fat diet （STZ-HFD） induced-type 2 diabetic rats and cells lines (L02 and HEK 293) to explore the mechanism of redox-mediated AMPK activation. We show glutaredoxins (Grxs) concomitant with optimal ROS act as an essential mediator for AMPK activation. ROS level results in different mechanisms for AMPK activation. Under low ROS microenvironment, Grxs-mediated S-glutathionylation on AMPK-α catalytic subunit activates AMPK to improve glucose transportation and degradation while inhibiting glycogen synthesis and keeping redox balance. While, under high ROS microenvironment, AMPK is activated by an AMP-dependent mechanism, however sustained high level ROS also causes loss of AMPK protein. This finding provides evidence for a new approach to diabetes treatment by individual doses of ROS or antioxidant calibrated against the actual redox level in vivo. Moreover, the novel function of Grxs in promoting glucose metabolism may provide new target for T2DM treatment.
DOI: 10.1016/j.freeradbiomed.2016.10.007
PubMed: 27743883
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Glutaredoxins concomitant with optimal ROS activate AMPK through S-glutathionylation to improve glucose metabolism in type 2 diabetes.</title><author><name sortKey="Dong, Kelei" sort="Dong, Kelei" uniqKey="Dong K" first="Kelei" last="Dong">Kelei Dong</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032, People's Republic of China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032</wicri:regionArea><wicri:noRegion>Shanghai 200032</wicri:noRegion></affiliation></author><author><name sortKey="Wu, Meiling" sort="Wu, Meiling" uniqKey="Wu M" first="Meiling" last="Wu">Meiling Wu</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032, People's Republic of China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032</wicri:regionArea><wicri:noRegion>Shanghai 200032</wicri:noRegion></affiliation></author><author><name sortKey="Liu, Xiaomin" sort="Liu, Xiaomin" uniqKey="Liu X" first="Xiaomin" last="Liu">Xiaomin Liu</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032, People's Republic of China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032</wicri:regionArea><wicri:noRegion>Shanghai 200032</wicri:noRegion></affiliation></author><author><name sortKey="Huang, Yanjie" sort="Huang, Yanjie" uniqKey="Huang Y" first="Yanjie" last="Huang">Yanjie Huang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032, People's Republic of China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032</wicri:regionArea><wicri:noRegion>Shanghai 200032</wicri:noRegion></affiliation></author><author><name sortKey="Zhang, Dongyang" sort="Zhang, Dongyang" uniqKey="Zhang D" first="Dongyang" last="Zhang">Dongyang Zhang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032, People's Republic of China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032</wicri:regionArea><wicri:noRegion>Shanghai 200032</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Yiting" sort="Wang, Yiting" uniqKey="Wang Y" first="Yiting" last="Wang">Yiting Wang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032, People's Republic of China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032</wicri:regionArea><wicri:noRegion>Shanghai 200032</wicri:noRegion></affiliation></author><author><name sortKey="Yan, Liang Jun" sort="Yan, Liang Jun" uniqKey="Yan L" first="Liang-Jun" last="Yan">Liang-Jun Yan</name><affiliation wicri:level="2"><nlm:affiliation>Department of Pharmaceutical Sciences, UNT System College of Pharmacy, University of North Texas Health Science Center, Fort Worth, TX, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pharmaceutical Sciences, UNT System College of Pharmacy, University of North Texas Health Science Center, Fort Worth, TX</wicri:regionArea><placeName><region type="state">Texas</region></placeName></affiliation></author><author><name sortKey="Shi, Dongyun" sort="Shi, Dongyun" uniqKey="Shi D" first="Dongyun" last="Shi">Dongyun Shi</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032, People's Republic of China. Electronic address: dyshi@fudan.edu.cn.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032</wicri:regionArea><wicri:noRegion>Shanghai 200032</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2016">2016</date><idno type="RBID">pubmed:27743883</idno><idno type="pmid">27743883</idno><idno type="doi">10.1016/j.freeradbiomed.2016.10.007</idno><idno type="wicri:Area/Main/Corpus">000400</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000400</idno><idno type="wicri:Area/Main/Curation">000400</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000400</idno><idno type="wicri:Area/Main/Exploration">000400</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Glutaredoxins concomitant with optimal ROS activate AMPK through S-glutathionylation to improve glucose metabolism in type 2 diabetes.</title><author><name sortKey="Dong, Kelei" sort="Dong, Kelei" uniqKey="Dong K" first="Kelei" last="Dong">Kelei Dong</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032, People's Republic of China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032</wicri:regionArea><wicri:noRegion>Shanghai 200032</wicri:noRegion></affiliation></author><author><name sortKey="Wu, Meiling" sort="Wu, Meiling" uniqKey="Wu M" first="Meiling" last="Wu">Meiling Wu</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032, People's Republic of China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032</wicri:regionArea><wicri:noRegion>Shanghai 200032</wicri:noRegion></affiliation></author><author><name sortKey="Liu, Xiaomin" sort="Liu, Xiaomin" uniqKey="Liu X" first="Xiaomin" last="Liu">Xiaomin Liu</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032, People's Republic of China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032</wicri:regionArea><wicri:noRegion>Shanghai 200032</wicri:noRegion></affiliation></author><author><name sortKey="Huang, Yanjie" sort="Huang, Yanjie" uniqKey="Huang Y" first="Yanjie" last="Huang">Yanjie Huang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032, People's Republic of China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032</wicri:regionArea><wicri:noRegion>Shanghai 200032</wicri:noRegion></affiliation></author><author><name sortKey="Zhang, Dongyang" sort="Zhang, Dongyang" uniqKey="Zhang D" first="Dongyang" last="Zhang">Dongyang Zhang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032, People's Republic of China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032</wicri:regionArea><wicri:noRegion>Shanghai 200032</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Yiting" sort="Wang, Yiting" uniqKey="Wang Y" first="Yiting" last="Wang">Yiting Wang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032, People's Republic of China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032</wicri:regionArea><wicri:noRegion>Shanghai 200032</wicri:noRegion></affiliation></author><author><name sortKey="Yan, Liang Jun" sort="Yan, Liang Jun" uniqKey="Yan L" first="Liang-Jun" last="Yan">Liang-Jun Yan</name><affiliation wicri:level="2"><nlm:affiliation>Department of Pharmaceutical Sciences, UNT System College of Pharmacy, University of North Texas Health Science Center, Fort Worth, TX, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pharmaceutical Sciences, UNT System College of Pharmacy, University of North Texas Health Science Center, Fort Worth, TX</wicri:regionArea><placeName><region type="state">Texas</region></placeName></affiliation></author><author><name sortKey="Shi, Dongyun" sort="Shi, Dongyun" uniqKey="Shi D" first="Dongyun" last="Shi">Dongyun Shi</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032, People's Republic of China. Electronic address: dyshi@fudan.edu.cn.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032</wicri:regionArea><wicri:noRegion>Shanghai 200032</wicri:noRegion></affiliation></author></analytic><series><title level="j">Free radical biology & medicine</title><idno type="eISSN">1873-4596</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>AMP-Activated Protein Kinases (genetics)</term><term>AMP-Activated Protein Kinases (metabolism)</term><term>Animals (MeSH)</term><term>Cell Line (MeSH)</term><term>Diabetes Mellitus, Experimental (etiology)</term><term>Diabetes Mellitus, Experimental (metabolism)</term><term>Diabetes Mellitus, Experimental (pathology)</term><term>Diabetes Mellitus, Experimental (prevention & control)</term><term>Diabetes Mellitus, Type 2 (metabolism)</term><term>Diabetes Mellitus, Type 2 (pathology)</term><term>Diet, High-Fat (adverse effects)</term><term>Epithelial Cells (cytology)</term><term>Epithelial Cells (metabolism)</term><term>Gene Expression Regulation (MeSH)</term><term>Glucose (metabolism)</term><term>Glutaredoxins (genetics)</term><term>Glutaredoxins (metabolism)</term><term>Glycogen (metabolism)</term><term>HEK293 Cells (MeSH)</term><term>Hepatocytes (cytology)</term><term>Hepatocytes (metabolism)</term><term>Humans (MeSH)</term><term>Liver (metabolism)</term><term>Liver (pathology)</term><term>Male (MeSH)</term><term>Oxidation-Reduction (MeSH)</term><term>Protein Subunits (genetics)</term><term>Protein Subunits (metabolism)</term><term>Rats (MeSH)</term><term>Rats, Sprague-Dawley (MeSH)</term><term>Reactive Oxygen Species (agonists)</term><term>Reactive Oxygen Species (antagonists & inhibitors)</term><term>Reactive Oxygen Species (metabolism)</term><term>Signal Transduction (MeSH)</term><term>Streptozocin (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>AMP-Activated Protein Kinases (génétique)</term><term>AMP-Activated Protein Kinases (métabolisme)</term><term>Alimentation riche en graisse (effets indésirables)</term><term>Animaux (MeSH)</term><term>Cellules HEK293 (MeSH)</term><term>Cellules épithéliales (cytologie)</term><term>Cellules épithéliales (métabolisme)</term><term>Diabète de type 2 (anatomopathologie)</term><term>Diabète de type 2 (métabolisme)</term><term>Diabète expérimental (anatomopathologie)</term><term>Diabète expérimental (métabolisme)</term><term>Diabète expérimental (prévention et contrôle)</term><term>Diabète expérimental (étiologie)</term><term>Espèces réactives de l'oxygène (agonistes)</term><term>Espèces réactives de l'oxygène (antagonistes et inhibiteurs)</term><term>Espèces réactives de l'oxygène (métabolisme)</term><term>Foie (anatomopathologie)</term><term>Foie (métabolisme)</term><term>Glucose (métabolisme)</term><term>Glutarédoxines (génétique)</term><term>Glutarédoxines (métabolisme)</term><term>Glycogène (métabolisme)</term><term>Humains (MeSH)</term><term>Hépatocytes (cytologie)</term><term>Hépatocytes (métabolisme)</term><term>Lignée cellulaire (MeSH)</term><term>Mâle (MeSH)</term><term>Oxydoréduction (MeSH)</term><term>Rat Sprague-Dawley (MeSH)</term><term>Rats (MeSH)</term><term>Régulation de l'expression des gènes (MeSH)</term><term>Sous-unités de protéines (génétique)</term><term>Sous-unités de protéines (métabolisme)</term><term>Streptozocine (MeSH)</term><term>Transduction du signal (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="agonists" xml:lang="en"><term>Reactive Oxygen Species</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Reactive Oxygen Species</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>AMP-Activated Protein Kinases</term><term>Glutaredoxins</term><term>Protein Subunits</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>AMP-Activated Protein Kinases</term><term>Glucose</term><term>Glutaredoxins</term><term>Glycogen</term><term>Protein Subunits</term><term>Reactive Oxygen Species</term></keywords><keywords scheme="MESH" qualifier="adverse effects" xml:lang="en"><term>Diet, High-Fat</term></keywords><keywords scheme="MESH" qualifier="agonistes" xml:lang="fr"><term>Espèces réactives de l'oxygène</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Diabète de type 2</term><term>Diabète expérimental</term><term>Foie</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Espèces réactives de l'oxygène</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Cellules épithéliales</term><term>Hépatocytes</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Epithelial Cells</term><term>Hepatocytes</term></keywords><keywords scheme="MESH" qualifier="effets indésirables" xml:lang="fr"><term>Alimentation riche en graisse</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Diabetes Mellitus, Experimental</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>AMP-Activated Protein Kinases</term><term>Glutarédoxines</term><term>Sous-unités de protéines</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Diabetes Mellitus, Experimental</term><term>Diabetes Mellitus, Type 2</term><term>Epithelial Cells</term><term>Hepatocytes</term><term>Liver</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>AMP-Activated Protein Kinases</term><term>Cellules épithéliales</term><term>Diabète de type 2</term><term>Diabète expérimental</term><term>Espèces réactives de l'oxygène</term><term>Foie</term><term>Glucose</term><term>Glutarédoxines</term><term>Glycogène</term><term>Hépatocytes</term><term>Sous-unités de protéines</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Diabetes Mellitus, Experimental</term><term>Diabetes Mellitus, Type 2</term><term>Liver</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Diabetes Mellitus, Experimental</term></keywords><keywords scheme="MESH" qualifier="prévention et contrôle" xml:lang="fr"><term>Diabète expérimental</term></keywords><keywords scheme="MESH" qualifier="étiologie" xml:lang="fr"><term>Diabète expérimental</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line</term><term>Gene Expression Regulation</term><term>HEK293 Cells</term><term>Humans</term><term>Male</term><term>Oxidation-Reduction</term><term>Rats</term><term>Rats, Sprague-Dawley</term><term>Signal Transduction</term><term>Streptozocin</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules HEK293</term><term>Humains</term><term>Lignée cellulaire</term><term>Mâle</term><term>Oxydoréduction</term><term>Rat Sprague-Dawley</term><term>Rats</term><term>Régulation de l'expression des gènes</term><term>Streptozocine</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">AMPK dysregulation contributes to the onset and development of type 2 diabetes (T2DM). AMPK is known to be activated by reactive oxygen species (ROS) and antioxidant interference. However the mechanism by which redox state mediates such contradictory result remains largely unknown. Here we used streptozotocin-high fat diet （STZ-HFD） induced-type 2 diabetic rats and cells lines (L02 and HEK 293) to explore the mechanism of redox-mediated AMPK activation. We show glutaredoxins (Grxs) concomitant with optimal ROS act as an essential mediator for AMPK activation. ROS level results in different mechanisms for AMPK activation. Under low ROS microenvironment, Grxs-mediated S-glutathionylation on AMPK-α catalytic subunit activates AMPK to improve glucose transportation and degradation while inhibiting glycogen synthesis and keeping redox balance. While, under high ROS microenvironment, AMPK is activated by an AMP-dependent mechanism, however sustained high level ROS also causes loss of AMPK protein. This finding provides evidence for a new approach to diabetes treatment by individual doses of ROS or antioxidant calibrated against the actual redox level in vivo. Moreover, the novel function of Grxs in promoting glucose metabolism may provide new target for T2DM treatment.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27743883</PMID><DateCompleted><Year>2017</Year><Month>12</Month><Day>29</Day></DateCompleted><DateRevised><Year>2019</Year><Month>12</Month><Day>27</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-4596</ISSN><JournalIssue CitedMedium="Internet"><Volume>101</Volume><PubDate><Year>2016</Year><Month>12</Month></PubDate></JournalIssue><Title>Free radical biology & medicine</Title><ISOAbbreviation>Free Radic Biol Med</ISOAbbreviation></Journal><ArticleTitle>Glutaredoxins concomitant with optimal ROS activate AMPK through S-glutathionylation to improve glucose metabolism in type 2 diabetes.</ArticleTitle><Pagination><MedlinePgn>334-347</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0891-5849(16)30449-X</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.freeradbiomed.2016.10.007</ELocationID><Abstract><AbstractText>AMPK dysregulation contributes to the onset and development of type 2 diabetes (T2DM). AMPK is known to be activated by reactive oxygen species (ROS) and antioxidant interference. However the mechanism by which redox state mediates such contradictory result remains largely unknown. Here we used streptozotocin-high fat diet （STZ-HFD） induced-type 2 diabetic rats and cells lines (L02 and HEK 293) to explore the mechanism of redox-mediated AMPK activation. We show glutaredoxins (Grxs) concomitant with optimal ROS act as an essential mediator for AMPK activation. ROS level results in different mechanisms for AMPK activation. Under low ROS microenvironment, Grxs-mediated S-glutathionylation on AMPK-α catalytic subunit activates AMPK to improve glucose transportation and degradation while inhibiting glycogen synthesis and keeping redox balance. While, under high ROS microenvironment, AMPK is activated by an AMP-dependent mechanism, however sustained high level ROS also causes loss of AMPK protein. This finding provides evidence for a new approach to diabetes treatment by individual doses of ROS or antioxidant calibrated against the actual redox level in vivo. Moreover, the novel function of Grxs in promoting glucose metabolism may provide new target for T2DM treatment.</AbstractText><CopyrightInformation>Copyright © 2016 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dong</LastName><ForeName>Kelei</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wu</LastName><ForeName>Meiling</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Xiaomin</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Huang</LastName><ForeName>Yanjie</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Dongyang</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Yiting</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yan</LastName><ForeName>Liang-Jun</ForeName><Initials>LJ</Initials><AffiliationInfo><Affiliation>Department of Pharmaceutical Sciences, UNT System College of Pharmacy, University of North Texas Health Science Center, Fort Worth, TX, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shi</LastName><ForeName>Dongyun</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Free Radical Regulation and Application Research Center of Fudan University, Shanghai 200032, People's Republic of China. Electronic address: dyshi@fudan.edu.cn.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>10</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Free Radic Biol Med</MedlineTA><NlmUniqueID>8709159</NlmUniqueID><ISSNLinking>0891-5849</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D021122">Protein Subunits</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017382">Reactive Oxygen Species</NameOfSubstance></Chemical><Chemical><RegistryNumber>5W494URQ81</RegistryNumber><NameOfSubstance UI="D013311">Streptozocin</NameOfSubstance></Chemical><Chemical><RegistryNumber>9005-79-2</RegistryNumber><NameOfSubstance UI="D006003">Glycogen</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="C568305">Prkaa1 protein, rat</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.31</RegistryNumber><NameOfSubstance UI="D055372">AMP-Activated Protein Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>IY9XDZ35W2</RegistryNumber><NameOfSubstance UI="D005947">Glucose</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D055372" MajorTopicYN="N">AMP-Activated Protein Kinases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003921" MajorTopicYN="N">Diabetes Mellitus, Experimental</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000517" MajorTopicYN="Y">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D059305" MajorTopicYN="N">Diet, High-Fat</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004847" MajorTopicYN="N">Epithelial Cells</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005947" MajorTopicYN="N">Glucose</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006003" MajorTopicYN="N">Glycogen</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D057809" MajorTopicYN="N">HEK293 Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D022781" MajorTopicYN="N">Hepatocytes</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008099" MajorTopicYN="N">Liver</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010084" MajorTopicYN="N">Oxidation-Reduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D021122" MajorTopicYN="N">Protein Subunits</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017207" MajorTopicYN="N">Rats, Sprague-Dawley</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName><QualifierName UI="Q000819" MajorTopicYN="N">agonists</QualifierName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013311" MajorTopicYN="N">Streptozocin</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">AMPK</Keyword><Keyword MajorTopicYN="Y">Glucose metabolism</Keyword><Keyword MajorTopicYN="Y">Glutaredoxins</Keyword><Keyword MajorTopicYN="Y">Glutathionylation</Keyword><Keyword MajorTopicYN="Y">ROS</Keyword><Keyword MajorTopicYN="Y">Type 2 diabetes</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>09</Month><Day>13</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2016</Year><Month>10</Month><Day>09</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>10</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>10</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>12</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>10</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27743883</ArticleId><ArticleId IdType="pii">S0891-5849(16)30449-X</ArticleId><ArticleId IdType="doi">10.1016/j.freeradbiomed.2016.10.007</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li><li>États-Unis</li></country><region><li>Texas</li></region></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Dong, Kelei" sort="Dong, Kelei" uniqKey="Dong K" first="Kelei" last="Dong">Kelei Dong</name></noRegion><name sortKey="Huang, Yanjie" sort="Huang, Yanjie" uniqKey="Huang Y" first="Yanjie" last="Huang">Yanjie Huang</name><name sortKey="Liu, Xiaomin" sort="Liu, Xiaomin" uniqKey="Liu X" first="Xiaomin" last="Liu">Xiaomin Liu</name><name sortKey="Shi, Dongyun" sort="Shi, Dongyun" uniqKey="Shi D" first="Dongyun" last="Shi">Dongyun Shi</name><name sortKey="Wang, Yiting" sort="Wang, Yiting" uniqKey="Wang Y" first="Yiting" last="Wang">Yiting Wang</name><name sortKey="Wu, Meiling" sort="Wu, Meiling" uniqKey="Wu M" first="Meiling" last="Wu">Meiling Wu</name><name sortKey="Zhang, Dongyang" sort="Zhang, Dongyang" uniqKey="Zhang D" first="Dongyang" last="Zhang">Dongyang Zhang</name></country><country name="États-Unis"><region name="Texas"><name sortKey="Yan, Liang Jun" sort="Yan, Liang Jun" uniqKey="Yan L" first="Liang-Jun" last="Yan">Liang-Jun Yan</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Bois/explor/GlutaredoxinV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000454 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 000454 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Bois
|area= GlutaredoxinV1
|flux= Main
|étape= Exploration
|type= RBID
|clé= pubmed:27743883
|texte= Glutaredoxins concomitant with optimal ROS activate AMPK through S-glutathionylation to improve glucose metabolism in type 2 diabetes.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:27743883" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \
| NlmPubMed2Wicri -a GlutaredoxinV1
| This area was generated with Dilib version V0.6.37. |  |