We used deconvolution analysis of 24-h plasma GH concentration profiles (10
- min sampling intervals) to appraise GH secretion rates and elimination ki
netics in obese (body mass index, similar to 34 kg/m(2)) premenopausal wome
n with large visceral fat area (LVFA, n = 8) us. small visceral fat area (S
VFA; n = 8) as determined by magnetic resonance imaging. The subjects were
matched for body mass index, body fat percentage, and age. The impact of th
e loss of 50% of prestudy weight excess induced by caloric restriction was
assessed as well. The results were compared with those obtained in normal w
eight control women (n = 8). LVFA subjects manifested markedly (4-fold) red
uced mean plasma GH levels, which was brought about by jointly diminished b
asal and pulsatile GH secretion. Moreover, visceral obesity was associated
with loss of regularity of GH release, as established by the approximate en
tropy statistic. In contrast, SVFA subjects produced normal daily amounts o
f GH and exhibited mean 24-h plasma GH concentrations that were similar to
those in normal weight controls: GH half-life and distribution volume were
not different among the study groups. Importantly, weight loss did not affe
ct the daily GH secretion rate in LVFA women, so that their mean plasma GH
concentration remained considerably reduced (similar to 50%) compared with
controls (despite the loss of similar to 40% of visceral fat). Normal GH ki
netics in SVFA women were not significantly influenced by weight reduction.
Thus, GH neuroregulation appears to be particularly altered in obese women
with a tendency to store fat in their visceral adipose depot. Because weig
ht loss did not reverse GH secretion rate in viscerally obese women, we spe
culate that relative hyposomatotropism is a primary feature of these women,
which could be involved in their tendency to preferentially store excess f
at in visceral adipose tissue.