Proteomic analysis of mitochondrial proteins of basal and lipolytically (isoproterenol and TNF-α)-stimulated adipocytes

The regulation of adipocyte lipolysis is increasingly believed to influence insulin resistance, in a process that may be associated with mitochondrial dysfunction. However, the molecular basis of the relationship between mitochondrial protein expression, lipolytic responsiveness, and insulin resista...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Journal of cellular biochemistry 2009-02, Vol.106 (2), p.257-266
Hauptverfasser: Cho, Si Young, Park, Pil Joon, Shin, Eui Seok, Lee, Jung Ho, Chang, Hui Kyoung, Lee, Tae Ryong
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:The regulation of adipocyte lipolysis is increasingly believed to influence insulin resistance, in a process that may be associated with mitochondrial dysfunction. However, the molecular basis of the relationship between mitochondrial protein expression, lipolytic responsiveness, and insulin resistance remains unknown. A set of proteins that shows altered abundances in the mitochondria of untreated and treated 3T3‐L1 adipocytes with TNF‐α or isoproterenol was identified. These include the proteins associated with energy production, including fatty acid oxidation, TCA cycle, and oxidative phosphorylation. Proteins associated with oxidative stress dissipation were down‐regulated in lipolytically stimulated adipocytes. Lipolytic stimulation with isoproterenol and TNF‐α, which is also a potent proinflammatory cytokine, showed some noticeable differences in mitochondrial protein expression. For example, isoproterenol markedly enhanced the expression of prohibitin which is involved in the integrity of mitochondria but TNF‐α did not. These results provide valuable information on mitochondrial dysfunction associated with oxidative stress induced by lipolytic stimulation. J. Cell. Biochem. 106: 257–266, 2009. © 2008 Wiley‐Liss, Inc.
ISSN:0730-2312
1097-4644
DOI:10.1002/jcb.21998