| Online-Ressource |
Verfasst von: | Mendler, Michael [VerfasserIn]  |
| Riedinger, Christin [VerfasserIn]  |
| Schlotterer, Andrea [VerfasserIn]  |
| Volk, Nadine [VerfasserIn]  |
| Fleming, Thomas [VerfasserIn]  |
| Herzig, Stephan [VerfasserIn]  |
| Nawroth, Peter Paul [VerfasserIn]  |
| Morcos, Michael [VerfasserIn]  |
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 |
Verf.angabe: | Michael Mendler, Christin Riedinger, Andrea Schlotterer, Nadine Volk, Thomas Fleming, Stephan Herzig, Peter P. Nawroth, Michael Morcos |
Jahr: | 2017 |
Umfang: | 7 S. |
Fussnoten: | Online 1 October 2016 ; Gesehen am 26.09.2018 |
Titel Quelle: | Enthalten in: Journal of diabetes and its complications |
Ort Quelle: | Amsterdam [u.a.] : Elsevier Science, 1992 |
Jahr Quelle: | 2017 |
Band/Heft Quelle: | 31(2017), 2, Seite 304-310 |
ISSN Quelle: | 1873-460X |
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. |
DOI: | doi:10.1016/j.jdiacomp.2016.09.014 |
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 |
| Volltext: http://www.sciencedirect.com/science/article/pii/S1056872716306365 |
| DOI: https://doi.org/10.1016/j.jdiacomp.2016.09.014 |
Datenträger: | Online-Ressource |
Sprache: | eng |
Sach-SW: | Diabetic neuropathy |
| Glycation/AGE |
| Insulin action |
| Longevity |
| Neuronal function |
| Oxidative stress/ROS |
K10plus-PPN: | 1581306288 |
Verknüpfungen: | → Zeitschrift |
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)