Adipose tissue disruption refers to the pathological alteration of fat cell (adipocyte) function and structure, leading to systemic metabolic dysfunction and chronic inflammation. This condition moves beyond simple fat storage to encompass impaired hormone secretion, particularly of adipokines like leptin and adiponectin. Clinically, it signifies a breakdown in the crucial endocrine role of fat tissue, contributing significantly to insulin resistance and cardiovascular risk.
Origin
The concept stems from foundational endocrinology and cellular physiology, where adipose tissue was reclassified from a passive energy depot to a highly active endocrine organ. The term ‘disruption’ highlights the shift from healthy, regulated lipid storage to a dysfunctional state marked by ectopic fat deposition and chronic low-grade inflammation. This clinical understanding has evolved with the increasing prevalence of metabolic syndrome.
Mechanism
Disruption is often initiated by chronic positive energy balance, resulting in adipocyte hypertrophy and subsequent hypoxia. This cellular stress triggers the release of pro-inflammatory cytokines, such as TNF-alpha and interleukin-6, which interfere with insulin signaling in peripheral tissues. Furthermore, the altered secretion of hormones from the dysfunctional adipocytes exacerbates systemic hormonal imbalance, directly impacting glucose homeostasis and overall physiological equilibrium.
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