title: Stress-related development of obesity and cortisol in women.
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 microg) significantly higher (P < 0.001) with respect to the NSRO (26.6 +/- 17.6 microg) or the normal-weight control groups (21.1 +/- 9.8 microg). Moreover, time (years) to achieve maximum Deltaweight gain (kg) and the Deltaweight 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 Deltaweight gain/time ratio. These findings support the concept that SRO has distinct pathophysiological mechanisms, including hyperactivity of the HPA axis.
authors.affiliation: Division of Endocrinology, Department of Internal Medicine, S. Orsola-Malpighi Hospital, University Alma Mater Studiorum of Bologna, Bologna, Italy.
authors.forename: Valentina
authors.initials: V
authors.lastname: Vicennati
authors.forename: Francesca
authors.initials: F
authors.lastname: Pasqui
authors.forename: Carla
authors.initials: C
authors.lastname: Cavazza
authors.forename: Uberto
authors.initials: U
authors.lastname: Pagotto
authors.forename: Renato
authors.initials: R
authors.lastname: Pasquali
mesh_terms: D015415:Biomarkers / Q000652:urine; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure; D015992:Body Mass Index; D016022:Case-Control Studies; D004032:Diet; D018450:Disease Progression; D015444:Exercise; D005260:Female; D012739:Gonadal Steroid Hormones / Q000097:blood; D006801:Humans; D006854:Hydrocortisone / Q000652:urine*; D007030:Hypothalamo-Hypophyseal System / Q000378:metabolism* / Q000503:physiopathology; D007328:Insulin / Q000097:blood; D008019:Life Style; D009765:Obesity / Q000097:blood / Q000503:physiopathology / Q000523:psychology*; D010913:Pituitary-Adrenal System / Q000378:metabolism* / Q000503:physiopathology; D017697:Premenopause; D012189:Retrospective Studies; D012738:Sex Hormone-Binding Globulin / Q000378:metabolism; D013315:Stress, Psychological / Q000097:blood / Q000150:complications* / Q000503:physiopathology; D013997:Time Factors; D015430:Weight Gain
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D012739:Gonadal Steroid Hormones; D007328:Insulin; D012738:Sex Hormone-Binding Globulin; D006854:Hydrocortisone