This clinical term refers to the age-related or hormonally mediated shift in the anatomical distribution of body fat. It typically involves a decrease in subcutaneous adipose tissue and a concurrent increase in visceral fat accumulation, particularly around the abdominal organs. This change in fat patterning is a significant indicator of metabolic health risk, often preceding or accompanying insulin resistance and dyslipidemia. Understanding this shift is central to preventative health strategies focused on longevity and endocrine balance.
Origin
The concept originates from clinical endocrinology and metabolic research, recognizing that the location of fat storage holds greater prognostic value than total body fat percentage alone. The terms ‘adipose tissue’ and ‘redistribution’ are derived from Latin and English, describing the movement of fatty connective tissue. Research into body composition changes during menopause and andropause solidified this as a distinct physiological phenomenon.
Mechanism
Hormonal fluctuations, primarily the decline in sex steroids like estrogen and testosterone, are key drivers in this process. Reduced estrogen, for instance, promotes lipogenesis in visceral depots while decreasing lipolysis in the gluteofemoral region. Cortisol, an adrenal hormone, also contributes by preferentially directing fat storage toward the central abdominal area under conditions of chronic stress. This visceral fat is metabolically active, releasing inflammatory adipokines that contribute to systemic inflammation and cardiovascular risk.
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