Adipose tissue visceralization describes the pathological process of fat deposition shifting from subcutaneous depots to the visceral compartment, accumulating around internal organs within the abdominal cavity. This specific distribution of adiposity is a clinically critical indicator, as visceral fat is metabolically active and highly secretory of pro-inflammatory adipokines. Increased visceralization is strongly associated with hormonal dysregulation, heightened cardiometabolic risk, and insulin resistance. The phenomenon is a key feature of central obesity and a major driver of chronic disease development.
Origin
The term derives from adipose, relating to fat, and visceral, referring to the internal organs of the body, combined with the suffix -ization, denoting a process of becoming or resulting in. The clinical distinction between subcutaneous and visceral fat gained prominence with advanced imaging techniques like CT and MRI, which allowed for precise quantification of this metabolically distinct fat depot. The recognition of visceral fat as an endocrine organ, rather than a passive energy store, solidified the importance of this specific distribution pattern in endocrinology and metabolism.
Mechanism
Visceralization is driven by a complex interplay of hormonal and genetic factors, notably chronic hypercortisolemia and altered sex steroid profiles, which favor the differentiation of pre-adipocytes into visceral fat cells. Visceral adipocytes possess a higher density of glucocorticoid and androgen receptors, making them more susceptible to stress hormones and less responsive to insulin. This fat depot exhibits enhanced lipolysis and portal drainage of free fatty acids directly to the liver, contributing to hepatic steatosis and dyslipidemia. Furthermore, visceral fat secretes a disproportionate amount of inflammatory cytokines, such as interleukin-6 and tumor necrosis factor-alpha, perpetuating systemic low-grade inflammation.
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