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Developmental Endocrinology Branch, National Institute of Child Health and Human Development Bethesda, Maryland 20892
Address all correspondence and requests for reprints to: Linda Liu, M.D., Developmental Endocrinology Branch, National Institute of Child Health and Human Development, Building 10, Room 10 N262, 9000 Rockville Pike, Bethesda, Maryland 20892.
Sex steroid administration can increase the GH response to provocative stimuli, but the relationship of sex steroids to spontaneous GH secretion is still controversial. We sought to characterize the effect of sex steroids on the plasma GH concentration by examining the 24-h pattern of episodic GH secretion in nine previously untreated adult men with isolated hypogonadotropic hypogonadism before and during long term testosterone, gonadotropin, or pulsatile GnRH treatment. After chronic sex steroid exposure, the mean 24-h plasma GH level, mean GH pulse amplitude, and mean area under the curve of pulses were significantly increased compared to pretreatment values [3.2 ± 1.8 (±SD) vs. 1,8 ± 1.2 ng/mL (P < 0.01); 11.4 ± 7.2 vs. 5.5 ± 4.4 ng/mL (P < 0.05); and 720 ± 547 vs. 316 ± 371 ng/mL·20 min (P < 0.05), respectively], while mean 24-h pre-arid posttreatment GH pulse frequencies were indistinguishable (5.7 ± 2.1 posttreatment vs. 5.0 ± 3.2 pretreatment; P = NS). The mean posttreatment plasma somatomedin-C level also rose significantly during treatment (1.89 ± 0.65 vs. 1.28 ± 0.48 U/mL; P < 0.01). We conclude that the increase in the mean plasma GH level during chronic sex steroid exposure is due mainly to augmentation of GH pulse amplitude, and that sex steroids probably increase spontaneous GH secretion.
Received July 17, 1986.
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