This describes the pathological shift in adipose tissue distribution where excess lipid storage preferentially accumulates around internal organs within the abdominal cavity, distinct from subcutaneous fat depots. This pattern is strongly associated with visceral adiposity, which functions as an endocrine organ promoting chronic inflammation and insulin resistance. It represents a critical marker of metabolic dysregulation.
Origin
‘Visceral’ pertains to the internal organs, ‘fat’ refers to adipose tissue, and ‘redistribution’ indicates a change in the location of this storage from peripheral to central sites. This phenomenon is often driven by dysregulated cortisol and sex hormone balance, linking it directly to endocrinology. The pattern itself carries significant prognostic weight.
Mechanism
High circulating cortisol levels, often associated with chronic stress, promote the differentiation of pre-adipocytes into visceral fat cells and enhance lipolysis in subcutaneous depots, directing free fatty acids centrally. Inadequate anabolic signaling further impairs the ability of muscle and subcutaneous tissue to utilize these fatty acids, forcing ectopic deposition. Reducing visceral load requires addressing the underlying endocrine drivers of this partitioning defect.
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