Deutsch
 
Benutzerhandbuch Datenschutzhinweis Impressum Kontakt
  DetailsucheBrowse

Datensatz

DATENSATZ AKTIONENEXPORT

Freigegeben

Zeitschriftenartikel

Adipose-Specific Deletion of TFAM Increases Mitochondrial Oxidation and Protects Mice against Obesity and Insulin Resistance.

MPG-Autoren

Vernochet,  Cecile
Max Planck Society;

Mourier,  Arnaud
Max Planck Society;

Bezy,  Olivier
Max Planck Society;

Macotela,  Yazmin
Max Planck Society;

Boucher,  Jeremie
Max Planck Society;

Rardin,  Matthew J
Max Planck Society;

An,  Ding
Max Planck Society;

Lee,  Kevin Y
Max Planck Society;

Ilkayeva,  Olga R
Max Planck Society;

Zingaretti,  Cristina M
Max Planck Society;

Emanuelli,  Brice
Max Planck Society;

Smyth,  Graham
Max Planck Society;

Cinti,  Saverio
Max Planck Society;

Newgard,  Christopher B
Max Planck Society;

Gibson,  Bradford W
Max Planck Society;

Larsson,  Nils-Göran
Max Planck Society;

Kahn,  C Ronald
Max Planck Society;

Volltexte (frei zugänglich)
Es sind keine frei zugänglichen Volltexte verfügbar
Ergänzendes Material (frei zugänglich)
Es sind keine frei zugänglichen Ergänzenden Materialien verfügbar
Zitation

Vernochet, C., Mourier, A., Bezy, O., Macotela, Y., Boucher, J., Rardin, M. J., et al. (2012). Adipose-Specific Deletion of TFAM Increases Mitochondrial Oxidation and Protects Mice against Obesity and Insulin Resistance. Cell Metab, 16(6), 765-776.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-0028-59E5-0
Zusammenfassung
Obesity and type 2 diabetes are associated with mitochondrial dysfunction in adipose tissue, but the role for adipose tissue mitochondria in the development of these disorders is currently unknown. To understand the impact of adipose tissue mitochondria on whole-body metabolism, we have generated a mouse model with disruption of the mitochondrial transcription factor A (TFAM) specifically in fat. F-TFKO adipose tissue exhibit decreased mtDNA copy number, altered levels of proteins of the electron transport chain, and perturbed mitochondrial function with decreased complex I activity and greater oxygen consumption and uncoupling. As a result, F-TFKO mice exhibit higher energy expenditure and are protected from age- and diet-induced obesity, insulin resistance, and hepatosteatosis, despite a greater food intake. Thus, TFAM deletion in the adipose tissue increases mitochondrial oxidation that has positive metabolic effects, suggesting that regulation of adipose tissue mitochondria may be a potential therapeutic target for the treatment of obesity.