A clinical state characterized by the deep abdominal adipose tissue, visceral fat, becoming metabolically dysfunctional, specifically exhibiting resistance to lipolysis, fat breakdown, despite caloric deficit and elevated resistance to the action of insulin. This resistance is a core feature of metabolic syndrome, leading to chronic systemic inflammation and the secretion of adverse adipokines that drive insulin resistance in other tissues. It represents a significant clinical challenge.
Origin
This term synthesizes concepts from endocrinology, particularly the study of insulin resistance, and adipocyte biology, focusing on the unique and pathological properties of visceral adipose tissue. Resistance highlights the failure of the fat cells to respond normally to metabolic signals. The clinical focus on visceral fat stems from its distinct anatomical location and its potent endocrine activity.
Mechanism
The mechanism involves chronic, low-grade inflammation within the visceral adipocytes, leading to the local release of inflammatory cytokines that interfere with the intracellular signaling pathways of both insulin and catecholamines. This inflammatory milieu prevents the efficient mobilization of stored triglycerides and simultaneously promotes the ectopic deposition of fat in organs like the liver and muscle, thereby propagating systemic metabolic dysfunction and hormonal imbalance.
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