Increased Cortisol Bioavailability, Abdominal Obesity, and the Metabolic Syndrome in Obese Women

Abstract

DUCLOS, MARTINE, PATRICIA MARQUEZ PEREIRA, PASCAL BARAT, BLANDIN GATTA, AND PATRICK ROGER. Increased cortisol bioavailability, abdominal obesity, and the metabolic syndrome in obese women. Obes Res. 2005;13:1157-1166. Objective: This study was conducted to obtain a detailed profile of hypothalamo-pituitary-adrenal (HPA) axis activity and reactivity and its differential relationships with body fat distribution and total fat mass in premenopausal obese women. Research Methods and Procedures:Cortisol responses to stimulation (awakening, food intake, exercise) and suppression (0.25 mg dexamethasone), cortisol metabolism, and tissue sensitivity to glucocorticoids were studied in 53 premenopausal obese women grouped according to their waist-to hip ratio: women with abdominal body fat distribution (A-BFD; n ϭ 31) and women with peripheral fat distribution (P-BFD; n ϭ 22). Results: Comparatively, A-BFD women had 1) lower awakening salivary cortisol levels; 2) increased salivary responsiveness to a standardized lunch; 3) similar pituitary sensitivity to dexamethasone but decreased sensitivity of monocytes to dexamethasone; 4) similar 24-hour urinary free cortisol but increased 24-hour urinary ratio of cortisone-to-cortisol; and 5) no difference in corticosteroid binding protein parameters.Discussion: Although abdominal obesity is not very different from generalized obesity in terms of HPA function, subtle variations in HPA axis activity and reactivity are evidenced in A-BFD premenopausal obese women.

Hypothalamic-pituitary-adrenal axis dysregulation and cortisol activity in obesity: A systematic review

“…Finally, a slightly different result emerged in a sample of obese women, where those with an abdominal body fat distribution (WHR > 0.85) had a similar CAR as those with a peripheral body fat distribution (WHR < 0.85). However, the actual salivary cortisol values were significantly lower at each time point among those with an abdominal body fat distribution (Duclos et al, 2005) Conversely, 3 studies found evidence in support of the opposite perturbation in CAR -an exaggerated response. One study, for example, found that CAR correlated positively with BMI, WHR, and sagittal diameter in men (Wallerius et al, 2003).…”

“…After a 0.0035 mg per kilogram body weight dose of dexamethasone, another sample of obese females did not differ from non-obese females in serum cortisol levels (Rask et al, 2002). Another sample of only females found that those with a WHR > 0.85 did not differ in feedback sensitivity, as indexed through plasma, from those with a WHR < 0.85 in response to a 0.25 mg dose of dexamethasone (Duclos et al, 2005). Finally, a study of both obese and normal BMI males and females found sex differences wherein obese females demonstrated significantly lower inhibition after dexamethasone doses of 0.0035 mg, 0.0070 mg, and 0.015 mg per kilogram of body weight, but that there were no differences in between obese and non-obese males (Pasquali et al, 2002).…”

“…One study that compared different distributions of body fat (abdominal versus peripheral) found that females with an abdominal body fat distribution (WHR > 0.85) showed no differences in 24-h UFC compared to those with peripherally distributed body fat (WHR < 0.85), but that they had a higher urinary cortisone:cortisol ratio (cortisone is the inactive 11-keto metabolite of cortisol; Duclos et al, 2005). A similar study found that females with an abdominal body fat distribution (WHR > 0.85) showed significantly lower UFC excretion than those with peripheral body fat distributions (WHR < 0.80; Vicennati and Pasquali, 2000).…”

“…For instance, one study of females found that those with an abdominal body fat distribution (WHR > 0.85) showed greater cortisol responsivity to eating lunch than those with a peripheral body fat distribution (WHR < 0.85; Duclos et al, 2005). A similar study found that obese females with an abdominal body fat distribution (WHR > 0.85), compared to those with a peripheral body fat distribution (WHR < 0.80) and to normal weight females, demonstrated greater cortisol concentrations in response to acute stressors (Vicennati and Pasquali, 2000).…”

11β-Hydroxysteroid Dehydrogenase Type 1 and the Metabolic Syndrome

“…Wang, 2011). It has been demonstrated that circulating cortisol concentrations are higher in patients with MetSyn compared with healthy subjects, both in basal conditions and during dynamic stimulation (Duclos et al, 2005;Misra et al, 2008;Phillips et al, 1998;Sen et al, 2008;Weigensberg et al, 2008). Furthermore, increased 11 -HSD1 activity in VAT may generate increased cortisol levels within AT and liver and thereby promote features of the MetSyn (Walker & Andrew, 2006).…”