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
Justin Hou Ming Yung et al. · Cells · 2020

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

This is one finding among thousands. Every one is graded and traced to its source, so you can see what the evidence actually supports. Browse the research →