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c-Jun N-terminal kinase pathways in diabetes

Authors
Journal
The International Journal of Biochemistry & Cell Biology
1357-2725
Publisher
Elsevier
Publication Date
Volume
40
Issue
12
Identifiers
DOI: 10.1016/j.biocel.2008.06.012
Keywords
  • Jnk
  • Insulin Resistance
  • Type 2 Diabetes
  • Lipid
Disciplines
  • Biology
  • Medicine

Abstract

Abstract Type 2 diabetes develops from insulin resistance and has become a worldwide epidemic. The c-Jun N-terminal kinases have been considered as signaling molecules linking inflammation and insulin resistance. Genetic disruption of c-Jun N-terminal kinase-1 gene prevents the development of insulin resistance in obese and diabetic mice. Inhibition of c-Jun N-terminal kinases by a small cell-permeable peptide improves insulin sensitivity in mice. Hepatic inhibition of c-Jun N-terminal kinases using a dominant-negative protein or knockdown of c-Jun N-terminal kinase-1 gene by RNA interference reduces blood glucose and insulin levels and enhances hepatic insulin signaling in mice. Recent evidence demonstrates that the hepatic c-Jun N-terminal kinase pathway plays an important role in lipid and lipoprotein homeostasis in mice. This review discusses recent advances in our understanding of the role of c-Jun N-terminal kinase pathway in metabolic control and its potential as a target for the treatment of type 2 diabetes.

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