Both oral and transdermal estrogen increase growth hormone release in postmenopausal women - A clinical research center study

To determine if the mode of 17β-estradiol (E₂) administration affects growth hormone (GH) concentrations, eight postmenopausal women were studied under the following conditions: (1) control (no E₂), (2) oral E₂ (Estrace, 1 mg every 12 h for 2 weeks) and (3) transdermal E₂ (Estraderm patch, 0.1 mg, two patches changed daily for 2 weeks). Blood was collected every 5 min for 24 h and assayed for serum GH concentrations using a sensitive chemiluminescence assay. Serum E₂ levels were comparable during both E₂ treatment regimens when measured with a specific chemiluminescence assay. The 24-h integrated GH concentrations (IGHC, min · μg/L) increased in all eight subjects from (mean ± SE) 494 ± 102 during control to 860 ± 111 (P < 0.05) and 832 ± 149 (P < 0.05) during oral and transdermal E₂, respectively. Both E₂ treatments significantly increased GH pulse height, individual pulse area, incremental pulse amplitude, interpeak valley concentration, and interpeak valley nadir (as measured by Cluster algorithm) when compared with control. No significant differences were observed in the number of GH pulses per 24 h. Insulin-like growth factor-I (IGF-I, μg/L) concentrations decreased from 165 ± 19 (control) to 109 ± 11 (oral E₂, P < 0.05) and 122 ± 15 (transdermal E₂, P < 0.05). No statistically significant differences in attributes of pulsatile GH release or IGF-I concentrations were observed between the oral and transdermal E₂ treatments. We conclude that both oral and transdermal E₂ treatment increase serum GH concentrations in postmenopausal women. This increase is manifested by larger GH pulses and higher basal (interpulse) GH levels, not by changes in pulse frequency. Both routes of E₂ administration decrease serum IGF-I concentrations, which may attenuate IGF-I negative feedback on pituitary somatotrophs and hypothalamic somatostatin secretion, resulting in enhanced pulsatile GH release.