Corticosteroid binding globulin gene polymorphism influences cortisol driven fat distribution in obese women.

Pascal Barat, Martine Duclos, Blandine Gatta, Patrick Roger, Pierre Mormede, Marie-Pierre Moisan
Obesity Research. 2005-09-01; 13(9): 1485-1490
DOI: 10.1038/oby.2005.179

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1. Obes Res. 2005 Sep;13(9):1485-90.

Corticosteroid binding globulin gene polymorphism influences cortisol driven fat
distribution in obese women.

Barat P(1), Duclos M, Gatta B, Roger P, Mormede P, Moisan MP.

Author information:
(1)Laboratory of Neurogenetics and Stress, INRA UMR 1243, University of Victor
Ségalen-Bordeaux 2, Bordeaux, France.

Hypothalamo-pituitary-adrenal axis has been reported to influence fat mass
distribution in obesity. We investigated the hypothesis that
corticosteroid-binding globulin (CBG) polymorphism could influence obesity,
metabolic, or hypothalamo-pituitary adrenal (HPA) axis activity parameters. In 44
obese pre-menopausal women, a microsatellite located within the CBG gene was
analyzed, providing three genotypes: 86/86 (n = 29), 86/90 (n = 14), and 90/90 (n
= 1). No significant difference was found for obesity, metabolic, and HPA axis
activity parameters between the genotypes 86/86 and 86/90. Looking for
differences in correlations between HPA axis activity parameters and obesity or
metabolic parameters between the two genotypes, genotype 86/90 showed a strong
correlation between salivary cortisol after dexamethasone (0.25 mg) suppression
test and waist-to-hip ratio (r = -0.84, p = 0.0007), whereas this correlation was
weaker for genotype 86/86 (r = -0.34, p = 0.09). These data were completed with
an analysis of the BclI polymorphism of the glucocorticoid receptor (GR) gene.
There was an association between this GR polymorphism and both awakening salivary
cortisol and postdexamethasone salivary cortisol but no association for obesity
or metabolic parameters. We concluded that CBG gene polymorphisms might modulate
the influence of the HPA axis on the fat mass distribution in this population.

DOI: 10.1038/oby.2005.179
PMID: 16222046 [Indexed for MEDLINE]

Auteurs Bordeaux Neurocampus