Program in Molecular Medicine
Biochemistry | Cell Biology | Cellular and Molecular Physiology | Molecular Biology
Obesity caused by feeding of a high-fat diet (HFD) is associated with an increased activation of c-Jun NH(2)-terminal kinase 1 (JNK1). Activated JNK1 is implicated in the mechanism of obesity-induced insulin resistance and the development of metabolic syndrome and type 2 diabetes. Significantly, Jnk1(-)(/)(-) mice are protected against HFD-induced obesity and insulin resistance. Here we show that an ablation of the Jnk1 gene in skeletal muscle does not influence HFD-induced obesity. However, muscle-specific JNK1-deficient (M(KO)) mice exhibit improved insulin sensitivity compared with control wild-type (M(WT)) mice. Thus, insulin-stimulated AKT activation is suppressed in muscle, liver, and adipose tissue of HFD-fed M(WT) mice but is suppressed only in the liver and adipose tissue of M(KO) mice. These data demonstrate that JNK1 in muscle contributes to peripheral insulin resistance in response to diet-induced obesity.
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DOI of Published Version
Mol Cell Biol. 2010 Jan;30(1):106-15. doi: 10.1128/MCB.01162-09. Epub . Link to article on publisher's site
Molecular and cellular biology
Sabio G, Kennedy NJ, Cavanagh-Kyros J, Jung D, Ko HJ, Ong H, Barrett T, Kim JK, Davis RJ. (2010). Role of muscle c-Jun NH2-terminal kinase 1 in obesity-induced insulin resistance. Davis Lab Publications. https://doi.org/10.1128/MCB.01162-09. Retrieved from https://escholarship.umassmed.edu/davis/78