Adipose tissue signaling disruption is a pathological state characterized by impaired or aberrant communication between body fat (adipose tissue) and distant metabolic organs, including the liver, muscle, and brain. This dysfunction involves a dysregulated secretion of critical adipokines, such as leptin and adiponectin, leading to a breakdown in systemic metabolic harmony. Clinically, this disruption is a key underlying contributor to chronic low-grade inflammation, systemic insulin resistance, and the unhealthy accumulation of visceral fat. Understanding this failure in endocrine communication is critical for addressing complex cardiometabolic risk profiles.
Origin
This clinical term originates from the field of endocrinology and metabolic research, stemming from the recognition of adipose tissue as a highly active endocrine organ rather than a passive energy storage depot. The core concepts of “signaling” and “disruption” are drawn from molecular biology and pathology, highlighting a functional failure within the body’s homeostatic communication network. It describes a profound impairment in the peripheral axes of the endocrine system.
Mechanism
The mechanism involves a detrimental shift in the secretory profile of adipocytes, particularly those within the visceral fat depots, moving away from beneficial, insulin-sensitizing adipokines toward pro-inflammatory cytokines like interleukin-6 and tumor necrosis factor-alpha. This altered hormonal output directly impairs insulin sensitivity in distant tissues and contributes to the pathological process of ectopic fat deposition. The resultant chronic inflammation and endocrine imbalance create a state of metabolic distress, interfering profoundly with glucose and lipid homeostasis throughout the body.
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