» Articles » PMID: 32183037

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

Overview
Journal Cells
Publisher MDPI
Date 2020 Mar 19
PMID 32183037
Citations 84
Authors
Affiliations
Soon will be listed here.
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.

Citing Articles

Insulin resistance and cancer: molecular links and clinical perspectives.

Caturano A, Erul E, Nilo R, Nilo D, Russo V, Rinaldi L Mol Cell Biochem. 2025; .

PMID: 40089612 DOI: 10.1007/s11010-025-05245-8.


Agomelatine Mitigates Kidney Damage in Obese Insulin-Resistant Rats by Inhibiting Inflammation and Necroptosis via the TNF-α/NF-ĸB/p-RIPK3 Pathway.

Promsan S, Pengrattanachot N, Phengpol N, Sutthasupha P, Thongnak L, Jaikumkao K Int J Mol Sci. 2025; 26(5).

PMID: 40076566 PMC: 11900133. DOI: 10.3390/ijms26051940.


Mitogen-Activated Protein Kinase Phosphatase-2 Deletion Promotes Hyperglycemia and Susceptibility to Streptozotocin-Induced Diabetes in Female Mice In Vivo.

Ghimire N, Welch M, Secunda C, Fink A, Lawan A Cells. 2025; 14(4).

PMID: 39996734 PMC: 11853640. DOI: 10.3390/cells14040261.


Unlocking the mechanistic potential of for managing diabetic neuropathy and nephropathy.

Singh S, Singh T J Tradit Complement Med. 2025; 14(6):581-597.

PMID: 39850604 PMC: 11752125. DOI: 10.1016/j.jtcme.2024.04.009.


High-fat diet mouse model receiving L-glucose supplementations propagates liver injury.

Amer J, Amleh A, Salhab A, Kolodny Y, Yochelis S, Saffouri B Front Nutr. 2025; 11:1469952.

PMID: 39742098 PMC: 11687001. DOI: 10.3389/fnut.2024.1469952.


References
1.
Kelpe C, Moore P, Parazzoli S, Wicksteed B, Rhodes C, Poitout V . Palmitate inhibition of insulin gene expression is mediated at the transcriptional level via ceramide synthesis. J Biol Chem. 2003; 278(32):30015-21. DOI: 10.1074/jbc.M302548200. View

2.
Engin A . The Pathogenesis of Obesity-Associated Adipose Tissue Inflammation. Adv Exp Med Biol. 2017; 960:221-245. DOI: 10.1007/978-3-319-48382-5_9. View

3.
Ozcan U, Cao Q, Yilmaz E, Lee A, Iwakoshi N, Ozdelen E . Endoplasmic reticulum stress links obesity, insulin action, and type 2 diabetes. Science. 2004; 306(5695):457-61. DOI: 10.1126/science.1103160. View

4.
Konstantynowicz-Nowicka K, Harasim E, Baranowski M, Chabowski A . New evidence for the role of ceramide in the development of hepatic insulin resistance. PLoS One. 2015; 10(1):e0116858. PMC: 4312035. DOI: 10.1371/journal.pone.0116858. View

5.
Blair A, Hajduch E, Litherland G, Hundal H . Regulation of glucose transport and glycogen synthesis in L6 muscle cells during oxidative stress. Evidence for cross-talk between the insulin and SAPK2/p38 mitogen-activated protein kinase signaling pathways. J Biol Chem. 1999; 274(51):36293-9. DOI: 10.1074/jbc.274.51.36293. View