OBESITY AND METABOLIC COMPLICATIONS - CONTRIBUTION OF DEHYDROEPIANDROSTERONE AND OTHER STEROID-HORMONES

Citation
A. Tchernof et al., OBESITY AND METABOLIC COMPLICATIONS - CONTRIBUTION OF DEHYDROEPIANDROSTERONE AND OTHER STEROID-HORMONES, Journal of Endocrinology, 150, 1996, pp. 155-164
Citations number
95
Categorie Soggetti
Endocrynology & Metabolism
Journal title
ISSN journal
00220795
Volume
150
Year of publication
1996
Supplement
S
Pages
155 - 164
Database
ISI
SICI code
0022-0795(1996)150:<155:OAMC-C>2.0.ZU;2-7
Abstract
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.