Research

Hormonal

Activation of the CML-RAGE axis in adipose tissue drives obesity-associated inflammation and insulin resistance by dysregulating adipokine expression (increasing pro-inflammatory cytokines and decreasing adiponectin).

This research suggests that obesity-related insulin resistance is driven by a specific molecular loop involving CML and RAGE in fat tissue. While this paper does not prescribe a direct intervention, it implies that reducing the formation of CML (an advanced glycation end product formed via lipid peroxidation) or blocking RAGE could theoretically improve insulin sensitivity. For now, strategies that reduce oxidative stress and lipid peroxidation (often associated with high sugar/fat diets) may indirectly mitigate this pathway.

GoodSupportsHIGH confidence
activation of the CML–RAGE axis plays an important role in obesity-associated inflammation and insulin resistance... CML induced a dysregulation of inflammatory adipokines in adipocytes via a RAGE-dependent pathway.
Katrien H.J. Gaens et al. · Arteriosclerosis Thrombosis and Vascular Biology · 2014

Why this rating

Strong evidence from human tissue, in vitro models, and genetically modified mouse models (RAGE-/-).

Source

N <sup>ε</sup> -(Carboxymethyl)lysine-Receptor for Advanced Glycation End Product Axis Is a Key Modulator of Obesity-Induced Dysregulation of Adipokine Expression and Insulin Resistance

Katrien H.J. Gaens et al. · Arteriosclerosis Thrombosis and Vascular Biology · 2014

DOI 10.1161/atvbaha.113.302281

mechanism_onlyCited 189×
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 →