Key result
Adiposopathy triggers systemic metabolic failure, MASLD, and hepatic insulin resistance via integrated adipose-organ communication networks.
Why the study?
The diagnostic landscape of obesity is transitioning from weight-centric metrics toward a functional clinical obesity framework.
This review highlights the pathophysiological mechanisms of adiposopathy and its role in driving systemic cardiometabolic illness through adipose-organ communication networks.
Answers are grounded in this paper and cite their sources.
May shift obesity assessment to functional metrics; leaves open validation in CV outcome trials.
The diagnostic landscape of obesity is transitioning from weight centric metrics toward a functional "clinical obesity" framework. This review explores the pathophysiology of adiposopathy ("sick fat"), where hypertrophic adipose tissue triggers systemic metabolic failure via the adipose-hepatic axis. Impaired subcutaneous adipose tissue (SAT) expandability, ectopic lipid accumulation, chronic inflammation, and maladaptive endocrine signaling are the hallmarks of adiposopathy ("sick fat"), a worldwide adipose tissue dysfunction. Through integrated adipose-organ communication networks, these changes support systemic cardiometabolic illness, MASLD, and hepatic insulin resistance. The molecular roles of DJ-1, Nrf2, and inflammatory kinases (JNK/IKKβ) in mediating this metabolic hit were examined in this study.
No takes yet. Share an insight, caveat, or question.
Sarvesh Sabarathinam (2026) conducted a review in Clinical obesity. Adiposopathy and hypertrophic adipose tissue trigger systemic metabolic failure, MASLD, and hepatic insulin resistance through integrated adipose-organ communication networks.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: