Actions of estrogen on pulsatile, nyctohemeral, and entropic modes of growth hormone secretion

The neuroendocrine mechanisms by which estradiol drives growth hormone (GH) secretion in the human are poorly defined. Here we investigate estrogen's specific regulation of the 24-h pulsatile, nyctohemeral, and entropic modes of GH secretion in healthy postmenopausal women. Volunteers (n = 9) receiv ed randomly ordered placebo versus estradiol-17 beta (1 mg micronized stero id twice daily orally) treatment for 7-10 days and underwent blood sampling at 10-min intervals for 24 h to capture GH release profiles quantitated in a high-sensitivity chemiluminescence assay. Pulsatile GH secretion was app raised via deconvolution analysis, nyctohemeral GH rhythms by cosinor analy sis, and the orderliness of GH release patterns via the approximate entropy statistic. Mean (+/-SE) 24-h serum GH concentrations approximately doubled on estrogen treatment (viz., from 0.31 +/- 0.03 to 0.51 +/- 0.07 mu g/l; P = 0.033). Concomitantly, serum insulin-like growth factor-I (IGF-I), lutei nizing hormone, and follicle-stimulating hormone concentrations fell, where as thyroid-stimulating hormone and prolactin levels rose (P < 0.01). The sp ecific neuroendocrine action of estradiol included I) a twofold amplified m ass of GH secreted per burst, with no significant changes in basal GH relea se, half-life, pulse frequency, or duration; 2) an augmented amplitude and mesor of the 24-h rhythm in GH release, with no alteration in acrophase; an d 3) greater disorderliness of CH release (higher approximate entropy). The se distinctive and dynamic reactions to estrogen are consistent with partia l withdrawal of IGF-I's negative feedback and/or accentuated central drive to GH secretion.