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Role of c-Jun N-terminal Kinase (JNK) in Obesity and Type 2 Diabetes

Authors
  • Yung, Justin Hou Ming
  • Giacca, Adria1, 2, 3
  • 1 Department of Medicine, University of Toronto, Toronto, ON M5S 1A8, Canada
  • 2 Institute of Medical Science, University of Toronto, Toronto, ON M5S 1A8, Canada
  • 3 Banting and Best Diabetes Center, University of Toronto, Toronto General Hospital, Toronto, ON M5S 2C4, Canada
Type
Published Article
Journal
Cells
Publisher
MDPI AG
Publication Date
Mar 13, 2020
Volume
9
Issue
3
Identifiers
DOI: 10.3390/cells9030706
PMID: 32183037
PMCID: PMC7140703
Source
PubMed Central
Keywords
License
Green

Abstract

Obesity has been described as a global epidemic and is a low-grade chronic inflammatory disease that arises as a consequence of energy imbalance. Obesity increases the risk of type 2 diabetes (T2D), by mechanisms that are not entirely clarified. Elevated circulating pro-inflammatory cytokines and free fatty acids (FFA) during obesity cause insulin resistance and ß-cell dysfunction, the two main features of T2D, which are both aggravated with the progressive development of hyperglycemia. The inflammatory kinase c-jun N-terminal kinase (JNK) responds to various cellular stress signals activated by cytokines, free fatty acids and hyperglycemia, and is a key mediator in the transition between obesity and T2D. Specifically, JNK mediates both insulin resistance and ß-cell dysfunction, and is therefore a potential target for T2D therapy.

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