OBJECTIVE: To determine whether delta 5-Androstene-3 beta,17 beta-diol or androstenediol secretion increases with body mass. DESIGN: A prospective study. SETTING: University-based clinical research center. PATIENTS: Twenty healthy, nonhirsute, eumenorrheic women, 10 with a body mass index (BMI) < 31 kg/m2 and 10 with a BMI > 31 kg/m2 were studied. INTERVENTIONS: All patients had blood sampled before (0 minute) and 60 minute after acute administration of 1 mg ACTH-(1-24) i.v. Body circumferences were obtained, and the BMI and waist-hip ratio was calculated. MAIN OUTCOME MEASURES: Total T, androstenedione (A), E2, sex hormone binding globulin, DHEA, DHEAS, and androstenediol were measured at 0 minutes (steroid 0): and DHEA, A and androstenediol were also measured after stimulation (steroid 60). The net steroid increment (delta) from 0 to 60 minute was calculated. RESULTS: Compared with thin women, obese subjects had higher levels of androstenediol 60 (95.8 +/- 20.3 versus 130.7 +/- 40.7 ng/dL, respectively [conversion factor to SI units, 0.03443]) and delta androstenediol (17.4 +/- 8.7 versus 37.8 +/- 29.0 ng/dL, respectively [conversion factor to SI units, 0.03443]). Neither the BMI, height, nor the body circumference measures correlated with any of the steroid levels or responses to adrenal stimulation, except for a weak positive correlation between BMI and estrone (E1) (r = 0.38) and a negative correlation between waist-hip ratio and delta androstenediol (r = -0.51). The basal level of T, E1, and DHEA0, but not A or DHEAS, correlated with androstenediol 0 (r = 0.65, 0.62, and 0.67, respectively) and delta androstenediol (r = 0.66, 0.63, and 0.63 to 0.005, respectively). CONCLUSIONS: Although the unstimulated morning androstenediol level did not differ between obese and thin euandrogenic healthy women, the response of androstenediol to ACTH-(1-24) stimulation was greater in obese individuals. The present findings, together with our previous data demonstrating an increased adrenal secretion of the E1 precursor A in response to ACTH in obese women, suggests that the adrenal cortex in overweight women may further enhance the estrogenic milieu of these women.
OBJECTIVE: To determine whether delta 5-Androstene-3 beta,17 beta-diol or androstenediol secretion increases with body mass. DESIGN: A prospective study. SETTING: University-based clinical research center. PATIENTS: Twenty healthy, nonhirsute, eumenorrheic women, 10 with a body mass index (BMI) < 31 kg/m2 and 10 with a BMI > 31 kg/m2 were studied. INTERVENTIONS: All patients had blood sampled before (0 minute) and 60 minute after acute administration of 1 mg ACTH-(1-24) i.v. Body circumferences were obtained, and the BMI and waist-hip ratio was calculated. MAIN OUTCOME MEASURES: Total T, androstenedione (A), E2, sex hormone binding globulin, DHEA, DHEAS, and androstenediol were measured at 0 minutes (steroid 0): and DHEA, A and androstenediol were also measured after stimulation (steroid 60). The net steroid increment (delta) from 0 to 60 minute was calculated. RESULTS: Compared with thin women, obese subjects had higher levels of androstenediol 60 (95.8 +/- 20.3 versus 130.7 +/- 40.7 ng/dL, respectively [conversion factor to SI units, 0.03443]) and delta androstenediol (17.4 +/- 8.7 versus 37.8 +/- 29.0 ng/dL, respectively [conversion factor to SI units, 0.03443]). Neither the BMI, height, nor the body circumference measures correlated with any of the steroid levels or responses to adrenal stimulation, except for a weak positive correlation between BMI and estrone (E1) (r = 0.38) and a negative correlation between waist-hip ratio and delta androstenediol (r = -0.51). The basal level of T, E1, and DHEA0, but not A or DHEAS, correlated with androstenediol 0 (r = 0.65, 0.62, and 0.67, respectively) and delta androstenediol (r = 0.66, 0.63, and 0.63 to 0.005, respectively). CONCLUSIONS: Although the unstimulated morning androstenediol level did not differ between obese and thin euandrogenic healthy women, the response of androstenediol to ACTH-(1-24) stimulation was greater in obese individuals. The present findings, together with our previous data demonstrating an increased adrenal secretion of the E1 precursor A in response to ACTH in obesewomen, suggests that the adrenal cortex in overweight women may further enhance the estrogenic milieu of these women.
Authors: S Yeh; H Y Kang; H Miyamoto; K Nishimura; H C Chang; H J Ting; M Rahman; H K Lin; N Fujimoto; Y C Hu; A Mizokami; K E Huang; C Chang Journal: Endocrine Date: 1999-10 Impact factor: 3.633
Authors: Stella Aslibekyan; Ellen W Demerath; Michael Mendelson; Degui Zhi; Weihua Guan; Liming Liang; Jin Sha; James S Pankow; Chunyu Liu; Marguerite R Irvin; Myriam Fornage; Bertha Hidalgo; Li-An Lin; Krista Stanton Thibeault; Jan Bressler; Michael Y Tsai; Megan L Grove; Paul N Hopkins; Eric Boerwinkle; Ingrid B Borecki; Jose M Ordovas; Daniel Levy; Hemant K Tiwari; Devin M Absher; Donna K Arnett Journal: Obesity (Silver Spring) Date: 2015-07 Impact factor: 5.002