Impact of mitochondrial ROS production in the pathogenesis of insulin resistance

Abstract Tumor necrosis factor-alpha (TNF-α) inhibits insulin action, in part, by activating c-jun NH2 -terminal kinases (JNK). However, the precise mechanisms by which TNF-α activates JNK are unknown. Recently, we confirmed that hyperglycemia increased mitochondrial reactive oxygen species (ROS) pr...

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Veröffentlicht in:	Diabetes research and clinical practice 2007-09, Vol.77 (3), p.S161-S164
Hauptverfasser:	Nishikawa, Takeshi, Kukidome, Daisuke, Sonoda, Kazuhiro, Fujisawa, Kazuo, Matsuhisa, Takako, Motoshima, Hiroyuki, Matsumura, Takeshi, Araki, Eiichi
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Apoptosis signal-regulating kinase 1 Endocrinology & Metabolism Glucose - pharmacology Humans Hyperglycemia - physiopathology Insulin - physiology Insulin resistance Insulin Resistance - physiology Mitochondria Mitochondria - drug effects Mitochondria - metabolism Models, Biological Reactive oxygen species Reactive Oxygen Species - metabolism Tumor necrosis factor-alpha Tumor Necrosis Factor-alpha - pharmacology Tumor Necrosis Factor-alpha - physiology
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