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Lee, H.Y.* ; Choi, C.S.* ; Birkenfeld, A.L.* ; Alves, T.C.* ; Jornayvaz, F.R.* ; Jurczak, M.J.* ; Zhang, D.* ; Woo, D.K.* ; Shadel, G.S.* ; Ladiges, W.* ; Rabinovitch, P.S.* ; Santos, J.H.* ; Petersen, K.F.* ; Samuel, V.T.* ; Shulman, G.I.*

Targeted expression of catalase to mitochondria prevents age-associated reductions in mitochondrial function and insulin resistance.

Cell Metab. 12, 668-674 (2010)
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Open Access Green as soon as Postprint is submitted to ZB.
Aging-associated muscle insulin resistance has been hypothesized to be due to decreased mitochondrial function, secondary to cumulative free radical damage, leading to increased intramyocellular lipid content. To directly test this hypothesis, we examined both in vivo and in vitro mitochondrial function, intramyocellular lipid content, and insulin action in lean healthy mice with targeted overexpression of the human catalase gene to mitochondria (MCAT mice). Here, we show that MCAT mice are protected from age-induced decrease in muscle mitochondrial function (∼30%), energy metabolism (∼7%), and lipid-induced muscle insulin resistance. This protection from age-induced reduction in mitochondrial function was associated with reduced mitochondrial oxidative damage, preserved mitochondrial respiration and muscle ATP synthesis, and AMP-activated protein kinase-induced mitochondrial biogenesis. Taken together, these data suggest that the preserved mitochondrial function maintained by reducing mitochondrial oxidative damage may prevent age-associated whole-body energy imbalance and muscle insulin resistance.
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Publication type Article: Journal article
Document type Scientific Article
ISSN (print) / ISBN 1550-4131
e-ISSN 1932-7420
Journal Cell Metabolism
Quellenangaben Volume: 12, Issue: 6, Pages: 668-674 Article Number: , Supplement: ,
Publisher Elsevier
Reviewing status Peer reviewed
Institute(s) Institute for Pancreatic Beta Cell Research (IPI)