Perimenopause Fat Distribution describes the characteristic shift in adipose tissue storage patterns observed in women during the transitional period leading up to menopause, typically moving from a gynoid (pear-shaped) pattern to an android (apple-shaped) or visceral fat accumulation pattern. This redistribution is clinically significant because increased visceral adiposity is a powerful, independent risk factor for metabolic syndrome, cardiovascular disease, and insulin resistance. This change is a direct consequence of fluctuating and declining ovarian hormone levels.
Origin
The term is derived from the endocrinology of aging, combining “perimenopause,” the period immediately preceding menopause, with the anatomical description of fat deposition. This pattern shift is a well-documented clinical observation that correlates closely with the loss of the protective metabolic effects of estrogen.
Mechanism
The mechanism is primarily driven by the progressive decline and erratic fluctuations of estrogen, specifically estradiol. Estrogen typically promotes subcutaneous fat storage and inhibits visceral fat accumulation by modulating the activity of fat-regulating enzymes and local cortisol action. As estrogen levels fall, this inhibitory effect is lost, leading to increased activity of the enzyme lipoprotein lipase in the visceral adipose tissue. Furthermore, the resulting relative androgen excess and changes in insulin sensitivity contribute to the preferential deposition of fat centrally around the abdominal organs.
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