title: Secretion of major adrenal androgens following ACTH administration in obese women with different body fat distribution.
abstract: To investigate whether obese female subjects with abdominal obesity may have adrenal androgen hypersecretion, we examined two groups of women with abdominal (n = 12) and peripheral (n = 13) obesity (defined by body mass index and waist-to-hip ratio) and a group of seven healthy normal-weight women. All subjects underwent the following protocol study that included a) baseline determination of major adrenal androgens, b) an ACTH test, performed by administering two boli of ACTH (Synacthen, 0.2 microg/Kg BW, e.v.), at 90 min intervals, with blood samples taken for cortisol and androgens, c) an oral glucose tolerance test, performed by administering glucose (75 gr), with blood samples taken for glucose and insulin determination. Each woman also underwent a control saline study. We then investigated the relationships between basal and stimulated androgen levels, body weight and fat distribution and fasting and stimulated insulin levels. Although basal cortisol levels were similar, their increase (as AUC) after the ACTH test was higher in women with abdominal obesity than in the other groups. On the contrary, there were no significant differences in basal and stimulated serum levels of dehydroepiandrosterone, androstenedione and 17-hydroxyprogesterone among the three groups. Fasting and stimulated (as AUC) insulin levels were significantly higher (p < 0.05) in women with abdominal obesity than in those with peripheral obesity and controls. No significant correlation was present between basal and stimulated androgen levels and body mass index, the waist-to-hip ratio or basal and stimulated cortisol values. Therefore, our data indicate that adrenal androgen secretion following low-dose ACTH administration in premenopausal women does not seem to be a function of body fat mass, fat distribution and insulin levels, nor does it correlate with the capacity of the adrenal glands to secrete cortisol in both basal and stimulated conditions.
authors.affiliation: Department of Internal Medicine and Gastroenterology, S. Orsola Hospital, University of Bologna, Italy.
authors.forename: V
authors.initials: V
authors.lastname: Vicennati
authors.forename: F
authors.initials: F
authors.lastname: Calzoni
authors.forename: A
authors.initials: A
authors.lastname: Gambineri
authors.forename: L
authors.initials: L
authors.lastname: Gagliardi
authors.forename: A M
authors.initials: AM
authors.lastname: Morselli Labate
authors.forename: F
authors.initials: F
authors.lastname: Casimirri
authors.forename: R
authors.initials: R
authors.lastname: Pasquali
mesh_terms: D019326:17-alpha-Hydroxyprogesterone / Q000097:blood; D000005:Abdomen; D000324:Adrenocorticotropic Hormone; D000328:Adult; D000728:Androgens / Q000378:metabolism*; D000735:Androstenedione / Q000097:blood; D001823:Body Composition; D001824:Body Constitution; D015992:Body Mass Index; D003687:Dehydroepiandrosterone / Q000097:blood; D005215:Fasting; D005260:Female; D005951:Glucose Tolerance Test; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007328:Insulin / Q000097:blood; D009765:Obesity / Q000503:physiopathology*
chemical_list: D000728:Androgens; D007328:Insulin; D000735:Androstenedione; D003687:Dehydroepiandrosterone; D019326:17-alpha-Hydroxyprogesterone; D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone