A. Tchernof et al., OBESITY AND METABOLIC COMPLICATIONS - CONTRIBUTION OF DEHYDROEPIANDROSTERONE AND OTHER STEROID-HORMONES, Journal of Endocrinology, 150, 1996, pp. 155-164
Obesity is a heterogeneous condition and not every obese patient is at
increased risk of cardiovascular diseases (CVD). It is now well estab
lished that the regional distribution of body fat is a critical correl
ate of the metabolic complications of obesity. Studies that have asses
sed adipose tissue distribution by imaging techniques such as computed
tomography have demonstrated the importance of the intra-abdominal (v
isceral) fat depot as a marker of a cluster of metabolic abnormalities
which include glucose intolerance, insulin resistance, hyper insuline
mia, hypertriglyceridemia, elevated number of apo B-carrying lipoprote
ins as well as hypoalphalipoproteinemia. Although the association betw
een visceral obesity and metabolic complications can hardly be questio
ned, it has been suggested that it may not necessarily represent a cau
sal relationship. For instance, concomitant alterations in sex steroid
levels have been found in both men and women with abdominal (visceral
) obesity which have also been reported to be significantly correlated
with the insulin resistant-dyslipidemic state found in abdominal obes
e subjects. In women, abdominal obesity is associated with increased f
ree testosterone concentrations and reduced sex hormone binding globul
in (SHBG) levels, whereas in men this condition is associated with red
uced testosterone and adrenal C-19 steroid (dehydroepiandrosterone, an
drostenedione, androstene-3 beta,17 beta-diol) levels as well as decre
ased SHBG concentrations. These altered steroid and SHBG levels have b
een reported to be independent correlates of the metabolic complicatio
ns of visceral obesity although they cannot solely account for the inc
reased CVD risk found in these patients. In this regard, intervention
studies are clearly warranted to better quantify the respective contri
bution of excess visceral adipose tissue and of the concomitant altera
tions in sex steroid levels as modulators of metabolic disturbances in
creasing CVD risk in obesity.