PuSH - Publication Server of Helmholtz Zentrum München: Reduction in <em>ins-7</em> gene expression in non-neuronal cells of high glucose exposed <em>Caenorhabditis elegans</em> protects from reactive metabolites, preserves neuronal structure and head motility, and prolongs lifespan.

Navigation

Home

Deutsch

Research

Advanced Search

Browse by ...

... Journal

... Publication Type

... Research Data

... Publication Year

Publication overview

Support & Contact

Contact persons

Help

Data protection

Mendler, M.* ; Riedinger, C.* ; Schlotterer, A.* ; Volk, N.* ; Fleming, T.* ; Herzig, S. ; Nawroth, P.P.* ; Morcos, M.*

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.

J. Diab. Complic. 31, 304-310 (2017)

Postprint

DOI

PMC

	Open Access Green

Abstract
Metrics
Extra information

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.

Altmetric

Additional Metrics?

[➜Log in]

Edit extra informations Login

Publication type Article: Journal article

Document type Scientific Article

Corresponding Author

Keywords Diabetic Neuropathy ; Glycation/age ; Insulin Action ; Longevity ; Neuronal Function ; Oxidative Stress/ros

ISSN (print) / ISBN 1056-8727

e-ISSN 1056-8727

Journal Journal of Diabetes and its Complications

Quellenangaben Volume: 31, Issue: 2, Pages: 304-310

Publisher Elsevier

Non-patent literature Publications

Reviewing status Peer reviewed

Institute(s) Institute of Diabetes and Cancer (IDC)