| |  Online-Ressource |
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| Verfasst von: | Mendler, Michael [VerfasserIn]  |
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| | Riedinger, Christin [VerfasserIn] |
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| | Schlotterer, Andrea [VerfasserIn] |
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| | Volk, Nadine [VerfasserIn] |
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| | Fleming, Thomas [VerfasserIn] |
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| | Herzig, Stephan [VerfasserIn] |
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| | Nawroth, Peter Paul [VerfasserIn] |
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| | Morcos, Michael [VerfasserIn] |
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| Titel: | Reduction in ins-7 gene expression in non-neuronal cells of high glucose exposed Caenorhabditis elegans protects from reactive metabolites, preserves neuronal structure and head motility, and prolongs lifespan |
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| Verf.angabe: | Michael Mendler, Christin Riedinger, Andrea Schlotterer, Nadine Volk, Thomas Fleming, Stephan Herzig, Peter P. Nawroth, Michael Morcos |
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| Jahr: | 2017 |
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| Umfang: | 7 S. |
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| Fussnoten: | Online 1 October 2016 ; Gesehen am 26.09.2018 |
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| Titel Quelle: | Enthalten in: Journal of diabetes and its complications |
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| Ort Quelle: | Amsterdam [u.a.] : Elsevier Science, 1992 |
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| Jahr Quelle: | 2017 |
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| Band/Heft Quelle: | 31(2017), 2, Seite 304-310 |
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| ISSN Quelle: | 1873-460X |
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| Abstract: | Background: Glucose derived metabolism generates reactive metabolites affecting the neuronal system and lifespan in C. elegans. Here, the role of the insulin homologue ins-7 and its downstream effectors in the generation of high glucose induced neuronal damage and shortening of lifespan was studied. Results: In C. elegans high glucose conditions induced the expression of the insulin homologue ins-7. Abrogating ins-7 under high glucose conditions in non-neuronal cells decreased reactive oxygen species (ROS)-formation and accumulation of methylglyoxal derived advanced glycation endproducts (AGEs), prevented structural neuronal damage and normalised head motility and lifespan. The restoration of lifespan by decreased ins-7 expression was dependent on the concerted action of sod-3 and glod-4 coding for the homologues of iron-manganese superoxide dismutase and glyoxalase 1, respectively. Conclusions: Under high glucose conditions mitochondria-mediated oxidative stress and glycation are downstream targets of ins-7. This impairs the neuronal system and longevity via a non-neuronal/neuronal crosstalk by affecting sod-3 and glod-4, thus giving further insight into the pathophysiology of diabetic complications. |
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| DOI: | doi:10.1016/j.jdiacomp.2016.09.014 |
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| URL: | Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.
Volltext: http://dx.doi.org/10.1016/j.jdiacomp.2016.09.014 |
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| | Volltext: http://www.sciencedirect.com/science/article/pii/S1056872716306365 |
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| | DOI: https://doi.org/10.1016/j.jdiacomp.2016.09.014 |
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| Datenträger: | Online-Ressource |
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| Sprache: | eng |
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| Sach-SW: | Diabetic neuropathy |
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| | Glycation/AGE |
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| | Insulin action |
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| | Longevity |
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| | Neuronal function |
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| | Oxidative stress/ROS |
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| K10plus-PPN: | 1581306288 |
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| Verknüpfungen: | → Zeitschrift |
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Reduction in ins-7 gene expression in non-neuronal cells of high glucose exposed Caenorhabditis elegans protects from reactive metabolites, preserves neuronal structure and head motility, and prolongs lifespan / Mendler, Michael [VerfasserIn]; 2017 (Online-Ressource)
