Stress‐related Development of Obesity and Cortisol in Women

Stress‐related Development of Obesity and Cortisol in Women Chronic exposure to environmental stress may play a role in the development of obesity, through hyperactivation of the hypothalamic–pituitary–adrenocortical (HPA) axis. This study investigated the dynamics of weight gain and the activity of the HPA axis in women who developed weight gain after a stressful event. This is a case–control retrospective study. Two groups of age‐matched premenopausal women were selected. One (n = 14) included women characterized by a rapid weight gain following a stressful event, defined as the “stress‐related obesity” (SRO) group, and the other (n = 21) women with nonstress‐related development of obesity, defined as the “nonstress‐related obesity” (NSRO) group. Twenty‐one healthy premenopausal women served as normal‐weight controls. Baseline hormonal and metabolic parameters, and 24‐h urinary free cortisol (UFC/24 h) excretion rate (as a measure of HPA‐axis activity) were measured in all women. Anthropometry, diet, and physical activity were similar in both obese groups. Both obese groups showed similar metabolic and hormonal profiles, but the SRO group had UFC/24 h values (41.1 ± 14.3 µg) significantly higher (P < 0.001) with respect to the NSRO (26.6 ± 17.6 µg) or the normal‐weight control groups (21.1 ± 9.8 µg). Moreover, time (years) to achieve maximum Δweight gain (kg) and the Δweight gain/time ratio were significantly shorter (P < 0.001) and higher (P < 0.001) in the SRO group with respect to the NSRO group, respectively. In the SRO group, there was a tendency to a significant correlation between UFC/24 h and the Δweight gain/time ratio. These findings support the concept that SRO has distinct pathophysiological mechanisms, including hyperactivity of the HPA axis. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Obesity Wiley

Stress‐related Development of Obesity and Cortisol in Women

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Publisher
Wiley
Copyright
2009 North American Association for the Study of Obesity (NAASO)
ISSN
1930-7381
eISSN
1930-739X
DOI
10.1038/oby.2009.76
pmid
19300426
Publisher site
See Article on Publisher Site

Abstract

Chronic exposure to environmental stress may play a role in the development of obesity, through hyperactivation of the hypothalamic–pituitary–adrenocortical (HPA) axis. This study investigated the dynamics of weight gain and the activity of the HPA axis in women who developed weight gain after a stressful event. This is a case–control retrospective study. Two groups of age‐matched premenopausal women were selected. One (n = 14) included women characterized by a rapid weight gain following a stressful event, defined as the “stress‐related obesity” (SRO) group, and the other (n = 21) women with nonstress‐related development of obesity, defined as the “nonstress‐related obesity” (NSRO) group. Twenty‐one healthy premenopausal women served as normal‐weight controls. Baseline hormonal and metabolic parameters, and 24‐h urinary free cortisol (UFC/24 h) excretion rate (as a measure of HPA‐axis activity) were measured in all women. Anthropometry, diet, and physical activity were similar in both obese groups. Both obese groups showed similar metabolic and hormonal profiles, but the SRO group had UFC/24 h values (41.1 ± 14.3 µg) significantly higher (P < 0.001) with respect to the NSRO (26.6 ± 17.6 µg) or the normal‐weight control groups (21.1 ± 9.8 µg). Moreover, time (years) to achieve maximum Δweight gain (kg) and the Δweight gain/time ratio were significantly shorter (P < 0.001) and higher (P < 0.001) in the SRO group with respect to the NSRO group, respectively. In the SRO group, there was a tendency to a significant correlation between UFC/24 h and the Δweight gain/time ratio. These findings support the concept that SRO has distinct pathophysiological mechanisms, including hyperactivity of the HPA axis.

Journal

ObesityWiley

Published: Sep 1, 2009

References

  • Glucocorticoid hormone binding to human adipose tissue
    Rebuffé‐Scrive, Rebuffé‐Scrive; Lundholm, Lundholm; Bjorntorp, Bjorntorp

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