Steroid hormones are implicated in the determination and maintenance of regional depots of adipose tissue in humans. This review focuses on the effects of steroids (estrogens, androgens, progestins and glucocorticoids) on fat distribution during growth and maturation. General and specific relationships that link androgens with android (abdominal) adiposity and estrogens with gynoid (gluteofemoral) adiposity are covered as they apply across the lifespan. Supporting relationships on steroid hormones and adipose tissue morphology include: adipogenesis and adipocyte hypertrophy and hyperplasia in puberty; regional adiposity in adults; aging and changes at menopause; regional differences in the cellular and metabolic characteristics of adipocytes, including lipoprotein lipase (LPL) activity and lipolysis, and the effects of steroids on these processes. At least in part, the distribution of adipose tissue in men and women appears to be determined by sex steroids. This generalization does not, however, entirely hold in obesity. This is because the additional adipose mass sequesters and produces steroids by aromatization: steroid metabolism varies throughout the body. In obese women, androgen/estrogen balance can account for adipose tissue distribution: such obesity involves a greater tissue exposure to unbound androgens, notably testosterone and dihydrotestosterone, due to reduced levels of sex hormone binding globulin (SHBG). Although lower in obese relative to non-obese women, SHBG is lower still in android obese than in gynoid obese women, tissue exposure to unbound androgens being greater for android obese women. Androgen/estrogen balance is not reflected by adipose tissue distribution in obese men who, despite a lowered androgen/estrogen ratio, tend to be android. Although many investigators have implied that cortisol is related to the distribution of adipose tissue in men and women, especially in obesity, the literature lends uneven support. If cortisol is related to adipose tissue distribution in normal individuals, it is perhaps through the differentiation of adipocyte precursors during adolescence and the induction of abdominal adipose tissue LPL activity, possibly through interactive effects with progesterone in women. Further investigation of relationships between steroid hormones and regional adiposity will prove invaluable for clarifying the known associations of adipose tissue distribution with disease risk, and documenting changes during normal growth, maturation and aging.
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