Research
Hormonal
Chronic activation of c-Jun N-terminal kinase (JNK) by elevated free fatty acids and pro-inflammatory cytokines during obesity causes insulin resistance and beta-cell dysfunction, leading to type 2 diabetes.
Obesity triggers a specific inflammatory response (JNK activation) that blocks insulin action. Managing obesity to reduce free fatty acids and inflammation is critical to preventing this molecular blockage.
GoodSupportsHIGH confidence
Elevated circulating pro-inflammatory cytokines and free fatty acids (FFA) during obesity cause insulin resistance and ß-cell dysfunction... 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
Why this rating
Based on a comprehensive review of multiple animal models (knockout mice) and human tissue studies.
Source
Role of c-Jun N-terminal Kinase (JNK) in Obesity and Type 2 Diabetes
Justin Hou Ming Yung et al. · Cells · 2020
DOI 10.3390/cells9030706
narrative_reviewCited 253×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
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