UMMS Affiliation
Program in Molecular Medicine
Publication Date
2010-01-01
Document Type
Article
Disciplines
Biochemistry | Cell Biology | Cellular and Molecular Physiology | Molecular Biology
Abstract
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.
Rights and Permissions
Publisher PDF posted as allowed by the publisher's author rights policy at http://journals.asm.org/site/misc/ASM_Author_Statement.xhtml.
DOI of Published Version
10.1128/MCB.01162-09
Source
Mol Cell Biol. 2010 Jan;30(1):106-15. doi: 10.1128/MCB.01162-09. Epub . Link to article on publisher's site
Journal/Book/Conference Title
Molecular and cellular biology
Related Resources
PubMed ID
19841069
Repository Citation
Sabio, Guadalupe; Kennedy, Norman J.; Cavanagh-Kyros, Julie; Jung, Dae Young; Ko, Hwi Jin; Ong, Helena; Barrett, Tamera; Kim, Jason K.; and Davis, Roger J., "Role of muscle c-Jun NH2-terminal kinase 1 in obesity-induced insulin resistance" (2010). Davis Lab Publications. 78.
https://escholarship.umassmed.edu/davis/78
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Biochemistry Commons, Cell Biology Commons, Cellular and Molecular Physiology Commons, Molecular Biology Commons