The Adipose–Organ Communication Network in Clinical Obesity: From Adiposopathy to Systemic Metabolic Failure

ABSTRACT

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.