The clinically significant, bidirectional relationship between chronically elevated levels of the stress hormone cortisol and the accumulation of metabolically active visceral fat, the fat stored deep within the abdominal cavity surrounding vital organs. High cortisol promotes the deposition of this specific, harmful fat type, which in turn increases systemic inflammation and further disrupts hormonal balance. This link is a key driver of metabolic syndrome and cardiovascular risk.
Origin
This concept is a cornerstone of metabolic endocrinology, rooted in studies of Cushing’s syndrome and the subsequent realization that chronic psychological stress mimics aspects of this disease. Research established that visceral adipose tissue possesses a higher density of glucocorticoid receptors and expresses enzymes that locally enhance cortisol activity. The term highlights a critical stress-metabolism nexus that must be addressed clinically.
Mechanism
Cortisol, a glucocorticoid, binds to receptors on adipocytes, particularly those in the visceral depot, promoting the differentiation of pre-adipocytes into mature fat cells and inhibiting lipolysis. Visceral fat then becomes an endocrine organ itself, releasing pro-inflammatory cytokines that impair insulin signaling and increase HPA axis activity. This creates a self-perpetuating cycle of stress, fat accumulation, and metabolic dysfunction that requires targeted intervention.
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