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

Détails

ID Serval
serval:BIB_0AD8CF7C3E94
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Targeted expression of catalase to mitochondria prevents age-associated reductions in mitochondrial function and insulin resistance.
Périodique
Cell Metabolism
Auteur(s)
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.
ISSN
1932-7420 (Electronic)
ISSN-L
1550-4131
Statut éditorial
Publié
Date de publication
2010
Volume
12
Numéro
6
Pages
668-674
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S.Publication Status: ppublish
Résumé
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.
Mots-clé
Adenosine Triphosphate/biosynthesis, Aging/metabolism, Animals, Catalase/genetics, Catalase/metabolism, DNA Damage, Energy Metabolism/physiology, Humans, Insulin/metabolism, Insulin Resistance/physiology, Male, Mice, Mice, Transgenic, Microscopy, Electron, Transmission, Mitochondria/metabolism, Mitochondria/physiology, Muscle, Skeletal/metabolism, Oxidative Stress/physiology, Oxygen Consumption/physiology, Reactive Oxygen Species/metabolism
Pubmed
Web of science
Open Access
Oui
Création de la notice
03/11/2015 13:32
Dernière modification de la notice
08/05/2019 14:13
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