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

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.

• Authors: Justin Hou Ming Yung, Adria Giacca
• Journal: Cells (Cells) Vol. 9 Issue 3 (03 13 2020) ISSN: 2073-4409 [Electronic] Switzerland
• PMID: 32183037 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

• Fatty Acids, Nonesterified
• Protein Kinase Inhibitors
• JNK Mitogen-Activated Protein Kinases
• Glucose

Topics

• Diabetes Mellitus, Type 2 (drug therapy, metabolism, pathology)
• Fatty Acids, Nonesterified (metabolism)
• Glucose (metabolism)
• Humans
• Inflammation
• Insulin Resistance
• Insulin Secretion
• JNK Mitogen-Activated Protein Kinases (antagonists & inhibitors, genetics, metabolism)
• Obesity (drug therapy, metabolism, pathology)
• Protein Kinase Inhibitors (therapeutic use)