Visceral Adiposity Drivers are the primary hormonal, genetic, and lifestyle factors that actively promote the preferential accumulation of metabolically active fat tissue deep within the abdominal cavity, surrounding the internal organs. These critical drivers include chronic hyperinsulinemia, sustained elevated cortisol exposure due to stress, and genetic predispositions that favor central fat storage over subcutaneous depots. Clinically, targeting these specific drivers is essential for reducing the high cardiovascular and metabolic risk profile associated with visceral adiposity.
Origin
A clinical and descriptive term combining ‘visceral adiposity,’ the metabolically hazardous fat around internal organs, and ‘drivers,’ the forces that cause movement or action. It emphasizes the multifactorial etiology of central obesity, moving beyond simple caloric excess to focus on underlying regulatory mechanisms.
Mechanism
Key hormonal drivers, such as chronic insulin resistance, directly shunt excess glucose and free fatty acids into visceral fat storage. High, sustained cortisol levels promote lipogenesis specifically in the visceral depot by increasing the expression of glucocorticoid receptors on these unique adipocytes. Furthermore, the visceral fat itself functions as a dysfunctional endocrine organ, releasing pro-inflammatory adipokines that exacerbate systemic inflammation and further impair insulin signaling, thereby creating a detrimental metabolic cycle.
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