In adults, abdominal visceral adiposity is related to an increased risk of
cardiovascular diseases, Type 2 diabetes mellitus, and stroke. The antecede
nts of these conditions likely begin with the alterations in body fat distr
ibution during childhood and adolescence. The sexually dimorphic alteration
s in fat distribution are influenced by sex differences in hormone concentr
ations, anatomical differences in the number and density of specific hormon
e receptors, capillary blood flow, and the activity of enzymes promoting li
pid synthesis or degradation. Hormones influencing the amount and regional
distribution of adipose tissue during puberty include cortisol, insulin, gr
owth hormone, and the sex steroids. Cortisol and insulin promote fat deposi
tion while the sex steroids and GH stimulate lipolysis. An overly sensitive
hypothalamic-pituitary-adrenal axis may exist in obesity and disrupt the b
alance between the lipogenic effects of cortisol and insulin and the lipoly
tic effects of sex steroids and growth hormone. Leptin is released from the
adipocytes and may act as a metabolic signal to the hypothalamic areas con
trolling satiety, energy expenditure, and the regulation of cortisol, insul
in, sex steroid and growth hormone release. The complex issues of the hormo
nal control of alterations in body fat distribution during puberty are deve
loped and a working model is proposed. (C) 1999 Wiley-Liss, Inc.