Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Impaired Insulin-/IGF1-Signaling Extends Life Span by Promoting Mitochondrial L-Proline Catabolism to Induce a Transient ROS-Signal

ABSTRACT: Transcriptome profiling of three models with impaired insulin/IGF1 signaling. 1. Deep sequencing of endogenous mRNA from Caenorhabditis elegans N2 var. Bristol (wildtype) and daf-2(e1370) mutant; 2. Deep sequencing of endogenous mRNA from murine embryonic fibroblasts (MEF) wildtype and irs1-/- knockout; 3. Deep sequencing of endogenous mRNA from murine embryoinic fibroblast (MEF) insr+/- -lox and insr+/- knockout 14 samples examined: C. elegans N2 var. Bristol (wildtype) vs. daf-2(e1370) mutant; MEF wildtype vs. irs1-/- knockout; MEF insr+/- -lox vs. insr +/- knockout

ORGANISM(S): Caenorhabditis elegans

SUBMITTER: Steffen Priebe 

PROVIDER: E-GEOD-36041 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Impaired insulin/IGF1 signaling extends life span by promoting mitochondrial L-proline catabolism to induce a transient ROS signal.

Zarse Kim K   Schmeisser Sebastian S   Groth Marco M   Priebe Steffen S   Beuster Gregor G   Kuhlow Doreen D   Guthke Reinhard R   Platzer Matthias M   Kahn C Ronald CR   Ristow Michael M  

Cell metabolism 20120401 4

Impaired insulin and IGF-1 signaling (iIIS) in C. elegans daf-2 mutants extends life span more than 2-fold. Constitutively, iIIS increases mitochondrial activity and reduces reactive oxygen species (ROS) levels. By contrast, acute impairment of daf-2 in adult C. elegans reduces glucose uptake and transiently increases ROS. Consistent with the concept of mitohormesis, this ROS signal causes an adaptive response by inducing ROS defense enzymes (SOD, catalase), culminating in ultimately reduced ROS  ...[more]

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